REVIEW

CLINICAL PRACTICE

Functional Movement Disorder: Evolving

Mechanisms, Diagnostic Precision, and
Personalized Multidisciplinary Care
Emmanuel Ortega-Robles, PhD,1 Ali Shalash, MD, PhD,2
n, MD, PhD1,4,*
Jesús Ramírez-Bermúdez, MD, PhD,3 and Oscar Arias-Carrio

Abstract: Background:
Background Functional movement disorder (FMD) is a neuropsychiatric condition characterized by
involuntary motor symptoms that are inconsistent with known neurological diseases and linked to dysfunction
in brain networks involved in motor control, emotion regulation, attention, and agency.
Objective To provide an updated and integrative review of the clinical, neurobiological, and therapeutic
Objective:
dimensions of FMD, incorporating recent evidence across diagnostic and treatment modalities.
Methods We conducted a comprehensive review of the leading studies on FMD, emphasizing the most
Methods:
common clinical presentations: functional tremor, dystonia, myoclonus, parkinsonism, gait disorder, and tics.
Drawing on recent evidence, we examined recovery-associated factors and integrated these insights into a
structured diagnostic and therapeutic algorithm.
Results FMD primarily affects women and typically presents with tremor, weakness, or mixed motor symptoms.
Results:
Phenotypic heterogeneity is common; non-motor symptoms such as pain, fatigue, and psychiatric comorbidities
contribute to clinical complexity. Neuroimaging and electrophysiological studies reveal salience, interoception,
and motor network disruptions, often involving the amygdala, sensorimotor cortex, and temporoparietal
junction. Diagnosis relies on positive clinical signs rather than exclusion. A five-phase diagnostic framework is
recommended, including neurological examination, patient-centred communication, and multidisciplinary
engagement. Treatment requires an individualized approach combining physiotherapy, cognitive behavioral
therapy, neuromodulation, pharmacotherapy, and digital tools. Prognosis varies, but early diagnosis, a strong
therapeutic alliance, and patient confidence in recovery improve outcomes.
Conclusions FMD is a multisystem disorder requiring integrated, personalized, and humanized care. Advances
Conclusions:
in neurobiology and therapeutic modalities offer promise, but unmet needs remain—particularly the
development of diagnostic biomarkers, standardized outcome measures, and scalable treatment models.

Functional Movement Disorder (FMD) is a common and often The diagnostic process has transitioned from an exclusion-
disabling condition seen across neurological practice. Historically based approach to one based on identifying positive clinical signs.
labeled as hysteria, psychogenic, dissociative, or conversion Misdiagnosis can lead to ineffective treatments and prolonged
disorder,1 FMD is now understood as a neuropsychiatric condition disability. Coexistence with structural neurological disorders adds
arising from the complex interaction of neurobiological, psychologi- to the diagnostic challenge.3
cal, and social factors. This redefined framework reflects advances in This narrative review summarizes current knowledge on the
neuroimaging and neurophysiology that demonstrate abnormalities epidemiology, pathophysiology, clinical features, and treatment
in brain networks involved in motor control, attention, emotion of FMD. It incorporates neuroimaging and electrophysiological
regulation, and self-agency without evidence of structural lesions.2 findings to describe the altered sensorimotor and affective

1
Experimental Neurology, Instituto Nacional de Rehabilitaci
on Luis Guillermo Ibarra Ibarra, Mexico City, Mexico; 2Department of Neurology, Faculty of Medicine, Ain
Shams University, Cairo, Egypt; 3Unidad de Neuropsiquiatría, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Su
arez, Mexico City, Mexico;
4
Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Mexico City, Mexico
*Correspondence to: Oscar Arias-Carri
on, Experimental Neurology, Instituto Nacional de Rehabilitaci

on Luis Guillermo Ibarra Ibarra. Mexico City
14389, Mexico. E-mail: ariasemc2@[Link]
Keywords: dystonia, functional movement disorder, prognosis, therapeutics, tremor.
Received 5 December 2024; accepted 25 April 2025.
Published online 00 Month 2025 in Wiley Online Library ([Link]). DOI: 10.1002/mdc3.70136

MOVEMENT DISORDERS CLINICAL PRACTICE 2025. doi: 10.1002/mdc3.70136

1
© 2025 International Parkinson and Movement Disorder Society.
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REVIEW INSIGHTS INTO FUNCTIONAL MOVEMENT DISORDER.

networks associated with symptoms. FMD is presented as a rates in girls.17 Tremor and dystonia remain the predominant
treatable neurological disorder, emphasizing the need for multi- subtypes.18,19
disciplinary and individualized management approaches that inte- FMD occurs less often in older adults. In a study of
grate scientific evidence with empathetic clinical care. 117 patients aged 62–70, only 18 developed symptoms after age
60. Tremor (61.1%) and dystonia (38.8%) were the most com-
mon, with identifiable stressors (mostly family-related) in 83.3%
and psychiatric comorbidities in 33.3%.20
Methods FMD frequently coexists with non-functional neurological disor-
ders (10–15% of cases).21,22 Known risk factors include sexual abuse,
A narrative approach was chosen due to the broad scope of the
post-traumatic stress disorder, alcohol misuse, suicide attempts, and
topic and the heterogeneity of available data. A structured search
significant psychosocial stressors such as divorce or
of PubMed identified peer-reviewed articles published between
bereavement.13,23–25 Social dynamics also modulate FMD incidence;
January 2015 and March 2025 using terms related to FMD and
the COVID-19 pandemic corresponded with increased FMD pre-
its subtypes. Eligible studies included original clinical research,
sentations in both pediatric and adult populations in the USA.26
interventional trials, and broader functional neurological disorder
(FND) studies with relevant data on motor manifestations.
Review articles, single case reports, and studies lacking methodo- Classification
logical transparency were excluded.
No standardized classification system currently exists for FMD.
The search yielded 1758 articles. Following exclusions,
Despite shared clinical features—variability, distractibility, and
324 studies remained, including 15 case series, 284 observational
inconsistency—it manifests across multiple phenotypes, including
studies, and 24 clinical trials. The final selection of articles was
tremor, weakness, dystonia, gait abnormalities, jerks, tics, and
based on the authors’ consensus. Further details are available in
myoclonus.
the Supplementary Material.
Subclassifying FMD into discrete phenotypes remains clini-
cally valuable, as subtypes differ in age of onset, sex distribution,
and treatment response.14 This “splitting” approach may reveal

Results phenotype-specific mechanisms and guide therapy. Support for

this framework comes from studies identifying distinct FMD
clusters. One analysis described two predominant subgroups: the
Epidemiology first included older patients with functional tremor and parkin-
FMD is more prevalent than historically recognized.4 Fahn sonism, often accompanied by anxiety and more responsive to
reported FMD in 0.6% of 2500 movement disorder patients, ris- pharmacological treatments. The second group comprised youn-
ing to 1.6% when including suspected functional origins. Among ger individuals with functional weakness, frequently reporting
1200 dystonia patients, 1.8% had a functional diagnosis.5 Ertan comorbid symptoms like headache, pain, and visual disturbances,
and colleagues found a prevalence of 2.8% in 1743 patients.6 and better managed with antidepressants.27
Stone et al reported that 15.5% of 3781 new neurology referrals However, the clinical relevance of this “splitting” model
met FND criteria, including 1.5% with FMD.7 Other studies remains debated. Tinazzi and colleagues reported substantial
estimate FMD affects 3–10% of new movement disorder clinic demographic and clinical characteristics overlap across FMD sub-
patients,8,9 and 5–10% of referrals without Parkinson’s dis- types, suggesting a shared pathophysiological basis.28 Furthermore,
ease.10,11 A recent cohort study reported that 18.3% (80 of 437) longitudinal data show that nearly half of the patients experience
of neurology patients had FND, including eight with FMD.12 shifts in their dominant movement disorder phenotype over time,
FMD occurs more frequently in women (2:1 to 5:1).5,6,13 challenging the stability and utility of rigid subtype classification.29
A meta-analysis including 4905 cases found 72.6% were female, Recent studies propose alternative frameworks that account
with mean onset at 39.6 years. Women present slightly earlier for both motor and non-motor dimensions. Gilmour et al intro-
than men (39.1 vs 41.0 years). The age distribution shows two duced a classification that distinguishes between episodic and
peaks: late adolescence (16–22 years) and midlife (35–45 years). constant symptom profiles.30 Patients with episodic FMD often
Common clinical presentations include mixed FMD (23.1%), exhibit hyperkinetic movements, anxiety, hyperarousal, and
tremor (21.6%), and weakness (18.1%). Functional dystonia trauma-related symptoms—features that may require trauma-
presents earlier (34.5 years), whereas gait disorder manifest later focused and emotion-regulation–based therapies. In contrast,
(43.2 years). While parkinsonism and myoclonus are more patients with constant FMD more commonly present with fixed
frequent in men, most subtypes predominate in women.14 dystonia, gait disturbance, and weakness, along with a reduced
Earlier reports suggested no racial or ethnic predisposition, but sense of agency and behavioral avoidance, supporting the use of
recent data highlight the need for a more detailed demographic motor retraining and psychologically informed rehabilitation.
analysis.9,14–16 Emerging classification systems may benefit from integrating
In pediatric populations, FMD mirrors adult presentations but clinical features—symptom profile, age at onset, psychiatric com-
may follow a more benign course with a better prognosis. orbidities, functional impairment—with biomarkers, including
Reported prevalence ranges from 2.8% to 23.1%, with higher amygdala reactivity and altered functional connectivity.31

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E. ORTEGA-ROBLES ET AL. REVIEW

A multidimensional approach may improve diagnosis, clarify frames FMD as a disorder influenced by predisposing, precipitat-
mechanisms, and guide personalized treatment. ing, and perpetuating factors rather than a purely neurological or
psychiatric condition (Fig. 1).32
Predisposing factors include abnormal sensorimotor integra-
Pathophysiology and tion, prior neurological illness, and genetic susceptibility. Psycho-
logical traits—particularly anxiety, depression, emotional
Etiopathogenesis dysregulation, and dissociative tendencies—contribute to symp-
FMD and other FND result from complex neurobiological, psy- tom development. Early-life trauma or adverse experiences
chological, and social interactions. The biopsychosocial model increase the risk, while acute stressors—injury, panic attacks, or

Figure 1. Neurobiological model of functional movement disorder (FMD). FMD arises from a complex interplay of predisposing and
precipitating factors, including psychiatric comorbidities, adverse life events, stress, physical trauma, and genetic or epigenetic
vulnerability. While no single causal pathway has been confirmed, mounting evidence implicates dysfunction across distributed brain
networks governing salience detection, interoception, agency, emotion regulation, and attentional control. These network abnormalities
manifest clinically as deficits in sensorimotor integration, emotional processing, and bodily awareness. Neuroimaging and
electrophysiological studies reveal alterations in activity and connectivity across key nodes, including the limbic system, motor cortex,
and regions involved in self-referential processing. Disruptions may involve hyperactivation, hypoactivation, and abnormal functional
coupling within and between networks. ACC, anterior cingulate cortex; Amy, amygdala; BG, basal ganglia; Cb, cerebellum; dlPFC,
dorsolateral prefrontal cortex; FEF, frontal eye fields; HC, hippocampus; Hyp, hypothalamus; IFC, inferior frontal cortex (gyrus); Ins, insula;
IPL, inferior parietal lobule; M1, primary motor cortex; OFC, orbitofrontal cortex; PAG, periaqueductal gray; PCC, posterior cingulate cortex;
PCu, precuneus; PHG, parahippocampal gyrus; S1, primary somatosensory cortex; SMA, supplementary motor area; SPL, superior parietal
lobule; Thal, thalamus; TPJ, temporoparietal junction; vmPFC, ventromedial prefrontal cortex.

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REVIEW INSIGHTS INTO FUNCTIONAL MOVEMENT DISORDER.

life events—often trigger onset. Maladaptive brain responses to pathophysiology. Structural and functional changes—including
pain, dysfunction, or uncertainty, along with social stressors such increased dendritic complexity and synaptic density—lead to
as financial instability, relational conflict, and lack of support, can excitatory-inhibitory imbalance and hyperactivity, disrupting
contribute to symptom persistence. Clinical reinforcement, includ- motor and executive control network regulation.32,36,47–54 Neuro-
ing extensive diagnostic testing to exclude structural disease, dis- imaging reveals hypoactivation of the contralateral primary motor
ability benefits, or the belief that symptoms are irreversible, may cortex and parietal regions, with concurrent hyperactivation in the
contribute to symptom worsening and chronicity.33,34 amygdala, temporoparietal junction, and insula.31 During emotion
Research on FND has identified abnormalities in sensory regulation tasks, FMD patients show increased activity in self-
processing, motor output, cognitive control, or combinations referential and interoceptive regions, suggesting altered self-
thereof, with FMD mainly affecting motor circuits.8,11,21,35 processing.55 Increased anterior cingulate cortex activation
Cognitive neuroscience highlights four core dysfunctions: altered correlates with emotional dysregulation and may predict treatment
attentional control, emotional dysregulation, impaired sensori- response.56,57 The enhanced amygdala-motor area connectivity
motor integration, and disrupted bodily self-awareness.36 These suggests limbic-motor coupling as a key mechanism underlying
dysfunctions implicate salience, agency, emotion regulation, and involuntary motor symptoms.
interoception networks. Whether these disruptions are Structural imaging studies report gray matter and subcortical
predisposing factors or consequences of chronic symptoms is volume differences—particularly in the basal ganglia, thalamus,
unclear, though a bidirectional model, where psychosocial stress and insula—associated with symptom severity, dissociation, and
alters brain function and reinforces maladaptive motor patterns, is childhood trauma.58 Machine learning models can distinguish
plausible.34,37 FND patients from controls based on neuroimaging data.59 In
Predictive coding models propose that FMD results from FMD, microstructural changes in limbic and associative tracts
disrupted integration of sensory input and motor predictions, suggest altered internal and external cues integration.60 Structural
leading to a reduced sense of agency.36 Affective and attentional differences in the temporoparietal junction and putamen may
biases shape prior expectations, which override top-down predic- relate to impaired self-agency and prediction error.59
tions and distort sensory processing. Electrophysiological and
behavioral data support this, showing cognitive biases favoring
expectations over sensory evidence.38 Slowed sensory processing Clinical Characteristics of
and reduced attention to interoceptive cues may enhance
feedforward errors. For example, individuals with functional dys-
Functional Movement Disorder
tonia show higher pain tolerance despite normal thresholds, indi- FMD presents with a broad spectrum of involuntary motor
cating a dissociation between sensory and emotional pain symptoms—including tremor, weakness, dystonia, gait abnor-
components.39 Heightened emotional salience may impair volun- malities, myoclonus, and tics—that are characteristically inconsis-
tary motor control, favoring automatic actions.40 Executive dys- tent, variable, and often incongruent with known structural
function, possibly from excessive attentional demands, may neurological diseases.35 Many patients demonstrate preserved
contribute to fatigue and concentration issues.41 Biomarkers have motor function under specific conditions, such as distraction or
been reported, such as absent contingent negative variation and dual-task testing, while emotional stimuli frequently exacerbate
reduced decision-making drift rate.38,42 Patients also show atten- symptoms.47
tional bias away from emotional faces and impaired impulse inhi- Despite ongoing debate on whether FMD should be concep-
bition.43,44 In functional gait disorder, maladaptive motor patterns tualized as a unitary disorder or a group of phenotypically distinct
and prolonged de-adaptation may stem from motor planning def- subtypes, subclassification remains clinically useful for diagnosis
icits and anxiety.45 and treatment.28 This review adopts a subtype-oriented
Functional neuroimaging shows altered connectivity in multi- perspective and describes the clinical features of the most com-
ple brain networks. Dorsal attention network disruption may mon phenotypes for educational and practical purposes.
impair goal-directed motor control. Sensorimotor and Despite this classification, mixed motor phenomenology
temporoparietal junction dysfunctions correlate with impaired remains the most frequent presentation. In a study by Gilmour
feedforward signaling and reduced agency. Salience and limbic and colleagues, more than half (53%) of patients exhibited more
network abnormalities are associated with interoceptive and than one motor symptom.30
emotional dysregulation. Ventral attention network deficits may Non-motor symptoms are also highly prevalent and contrib-
compromise stimulus-driven attention.36 ute significantly to disability. Pain (84%) and fatigue (65%) are
FND patients show increased limbic reactivity to emotional common across all motor phenotypes.30 Psychiatric com-
stimuli, including heightened amygdala activation, elevated cortisol orbidities, especially anxiety, depression, and trauma-related
levels, and altered heart rate variability.34,46 Failure to habituate to symptoms, are also frequent.
negative stimuli may contribute to persistent stress responses.47 Tinazzi et al reported that 45.8% of patients had combined
Dysregulated midbrain and prefrontal regions activation during movement phenotypes, and 83.9% experienced at least one non-
emotional tasks suggest impaired behavioral–motor responses to motor symptom, most commonly anxiety (52.1%), fatigue
perceived threats. The amygdala, influenced by early-life (45.1%), and pain (41.9%).61 In a separate study, pain was more
trauma and cortisol exposure, plays a central role in FMD frequent in functional dystonia (47.4%) than in functional tremor

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E. ORTEGA-ROBLES ET AL. REVIEW

(17.5%). Functional weakness was associated with a higher preva- seminal case series by Fahn and Williams and Lang provided
lence of sensory disturbances (51.7%) compared to tremor insights into its clinical presentation. Fahn and Williams described
(7.5%), dystonia (5.3%), or gait disorder (11.8%).28 39 patients (mean age 26 years, SD 13.6; two male), including
Other non-motor features—including insomnia, dissociative seven with paroxysmal and 14 with continuous dystonia. Com-
symptoms, and depersonalization—also contribute to the clinical mon features included inconsistent dystonic postures (18 patients),
profile, although their prevalence does not appear to differ sub- functional weakness (14), sensory disturbances (5), somatization
stantially across motor subtypes. These findings underscore the symptoms (8), functional seizures (5), and co-occurring FMD
importance of a holistic diagnostic framework that considers both (7). Nine achieved complete remission, and four showed signifi-
motor and non-motor dimensions of FMD and the high degree cant improvement.74 Lang’s series (18 patients, mean age
of clinical overlap across subtypes. 35.5 years, SD 12.7; five male) reported focal onset dystonia in
15 cases, with 14 identifying a precipitating event. Nine had
acute symptom onset, 10 exhibited other functional motor
Functional Tremor symptoms, and 15 had functional neurological comorbidities.77
Functional tremor, the most common FMD subtype, represents Functional dystonia typically presents with fixed, abnormal
40–50% of cases in specialist clinics.5,6,8,11,18,21,62 A meta-analysis postures, sometimes following minor trauma. Diagnosis relies on
found it in 21.6% of FMD patients, with a female predominance positive clinical features such as inconsistency and variability
of 72.9%.14 Unlike non-functional tremors, it presents with (Table 1).78–80
rhythmic, involuntary jerks, typically of sudden onset and non- Recent studies continue to investigate the neurophysiological
progressive course. Clinical features include spontaneous basis of functional dystonia. In functional torticollis, EMG
remissions, paroxysmal exacerbations, the coexistence of rest, recordings show abnormal autospectral peaks in the
postural and action tremors, and fluctuating frequency and sternocleidomastoid and splenius muscles, which are not seen in
amplitude.63–70 Symptoms are often modulated by cognitive or non-functional cases.81 Espay et al reported that patients with
emotional factors, serving as diagnostic clues. functional dystonia have altered cortical and spinal excitability
Tremor usually affects the limbs bilaterally and symmetrically, similar to structural dystonia, suggesting possible shared
with frequencies ranging from 4 to 10 Hz, and may involve the mechanisms.82
head or voice. Coexisting functional movement symptoms,
including dystonia and myoclonus, are common, while associa-
tions with functional parkinsonism, tics, or dyskinesias are less
frequent.68–70
Functional Myoclonus
Functional tremor often intensifies with focused attention and Functional myoclonus is characterized by involuntary, irregular
improves with distraction, although this can also occur in parkin- jerks with variable amplitude, frequency, and distribution, unlike
sonian tremor. A key feature is the coactivation sign, where ago- the consistent patterns in structural myoclonus. Monday and
nist and antagonist muscles activate simultaneously, leading to Jankovic’s study of 18 patients (mean age 49.5 years) found seg-
irregular, jerky, or inconsistent movements.65 Another hallmark mental myoclonus in 10, generalized in 7, and focal in 1. Onset
is entrainment, where tremor frequency synchronizes with vol- was abrupt in most (n = 11), with symptoms worsening under
untary rhythmic tasks, such as finger tapping. Functional tremor stress (n = 15). Distraction improved symptoms in 14 patients
may spread to adjacent body parts or generalize but rarely affect and placebo in 9, suggesting modifiability as a diagnostic clue.83
the fingers.64 Exaggerated slowness and inconsistency across tasks, Functional axial jerks represent a common manifestation.84
sometimes called the “whack-a-mole sign,” can also aid Electrophysiological studies aid in distinguishing functional
diagnosis. from structural myoclonus. EMG shows prolonged muscle bursts
Electrophysiological assessments, such as electromyography (>100 ms), no triphasic activation between agonist and antago-
and accelerometry, often show marked amplitude, direction, and nist muscles, and delayed latencies, contrasting with the short,
frequency variability.71 Approximately half of the patients have synchronized bursts of cortical or subcortical myoclonus.85
tremor rhythm coherence across muscle groups.72 The Bereitschaftspotential (BP), a pre-movement cortical
potential, can also support the diagnosis. The BP includes an
early component associated with motor intention and planning
Functional Dystonia
and a late component related to execution.86 In patients with
Functional dystonia is the second most common phenotype of functional myoclonus, a BP preceding jerks suggests voluntary
FMD, though some reports place it third after myoclonus. Its motor preparation, supporting functional etiology.87 However,
diagnosis is challenging due to the lack of definitive biomarkers the clinical utility of BP is limited by its relatively low sensitivity.
to distinguish it from idiopathic dystonia, often leading to mis- In one study, BP was detectable in only 63% of cases,88 demon-
classification. Initial reports on functional dystonia emerged in strating high specificity but restricting its standalone diagnostic
1975, with case presentations at the 1983 American Academy of value.89 Consequently, the diagnosis of functional myoclonus
Neurology meeting.73 remains primarily clinical, guided by the presence of positive
Estimates suggest functional dystonia accounts for 2.2% to signs such as variability, distractibility, and entrainment, and
12% of dystonia cases and 11.8% of FMD patients.14,74–76 Two supported by electrophysiological findings when available.

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REVIEW INSIGHTS INTO FUNCTIONAL MOVEMENT DISORDER.

TABLE 1 Clinical features supporting a diagnosis of Functional Movement Disorder

Patient history Physical examination

• Sudden or abrupt symptom onset Inconsistency

• Clear triggers such as physical injury, illness, or psychological • Variability: Movement characteristics (eg, tremor amplitude or
stressors frequency) change across time or context
• Spontaneous remissions or marked symptom fluctuations • Distractibility: Symptoms diminish or resolve when attention is
• History of childhood trauma or adverse life events diverted (eg, mental arithmetic)
• Psychiatric comorbidities (eg, anxiety, depression, PTSD) • Suggestibility: Symptom intensity alters in response to verbal
• Family history of functional neurological or psychiatric disorders suggestion or clinician focus
• Detailed, emotionally charged descriptions of symptom onset • Selectivity: Symptoms manifest only in specific contexts (eg,
clinical exam) but not in everyday function
Incongruence (Positive Signs)
• Entrainment: Tremor aligns with the rhythm of voluntary
movement in another limb
• Hoover’s sign: Apparent weakness in hip extension improves
during contralateral resisted hip flexion
• Fixed postures with resistance: Involuntary toe posturing resistant
to passive manipulation (eg, “functional toe sign”)
• Whack-a-mole sign: Inhibiting one movement leads to the
emergence of a different body part
• Swivel chair sign: Patient unable to walk can propel a chair using
legs while seated

Functional Parkinsonism narrow-base “tightrope” gait, stiff “robot-like” gait, limping,

choreiform movements, and theatrical or unusual patterns like
Functional parkinsonism, a rare and challenging phenotype of walking on a “sticky surface” or through water.11
FMD, was first described in 1988.90 It remains under-recognized Rubino later categorized FGD as a higher-level gait disorder,
due to its clinical overlap with neurodegenerative parkinsonian alongside cautious gait, frontal lobe gait disorders, gait initiation
syndromes and variable presentation. Lang et al reported 14 cases failure, and primary progressive freezing of gait.96 In 60 cases,
(7 male), most showing features of functional parkinsonism, Keane found ataxic gait most common (40%), followed by
including rest tremor with inconsistent frequency (12 patients), hemiparetic (21.7%), paraparesis-like (16.7%), and tremulous
rigidity reflecting voluntary resistance (6), and incongruent gaits (18%).97 Baik and Lang, in a larger cohort (n = 279), noted
bradykinesia, gait disturbances, or postural instability (12).91 that excessive slowness, including in gait, was more common in
Key clinical signs include slowness during repetitive move- pure FMD cases.98
ments, lacking the decremental pattern of idiopathic Parkinson’s Characteristic features of FGD include variability with sugges-
disease, variable resistance to passive movement without cogwheel tion or distraction, excessive slowness or hesitation, exaggerated
rigidity, and exaggerated effort (the “huffing and puffing” sign). unsteadiness without falling, and signs like a functional Romberg
These features and fixed postures suggest a functional origin rather (marked swaying without sensory or vestibular deficits), “walk-
than structural parkinsonism.92 ing-on-ice” gait (short, cautious steps with stiff knees and ankles),
Functional parkinsonism can co-occur with idiopathic and sudden knee buckling without true collapse.99–101
Parkinson’s disease, complicating diagnosis as functional symp- While diagnosis is primarily clinical, ancillary tools—such as
toms may mask structural pathology.93–95 Accurate diagnosis stabilometry, posturography, and vertical plane kinematic
relies on a thorough clinical assessment supported by electrophys- analysis—can help distinguish FGD from subtle cerebellar, sen-
iological studies and, when needed, SPECT imaging. With care- sory, or pyramidal disorders.102–104
ful longitudinal observation, diagnosis remains primarily clinical, FGD often coexists with other FMD and non-motor symp-
focusing on signs of inconsistency, variability, and distractibility. toms like fatigue, pain, or dissociation. Recognition of inconsis-
tency and incongruence through focused neurological
examination is key for diagnosis.
Functional Gait Disorder
Functional gait disorder (FGD) involves abnormal walking pat-
terns without a consistent neurological basis and remains diag-
Functional Tics
nostically challenging due to their variability. Although no
standardized classification exists, early descriptions by Roussy and Functional tics have gained attention due to a notable rise in
Lhermitte included patterns such as astasia-abasia, pseudotabetic cases following the COVID-19 pandemic, particularly among
gait, and pseudopolyneuritic gait. Other reported types include adolescents and young adults.105–107 Defined as sudden, rapid,

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E. ORTEGA-ROBLES ET AL. REVIEW

recurrent, non-rhythmic motor movements or vocalizations

without a structural basis,108 their pre-pandemic prevalence was
Diagnosis
estimated at 4–5% of FMD cases,6,108,109 though recent studies The diagnostic approach to FMD has evolved significantly from
report rates from 2% to 32%, depending on criteria.109,110 Many exclusion to a rule-in strategy based on positive signs, improving
cases present acutely, often in females, following psychosocial confidence and enabling earlier intervention.
stressors.111 In 1988, Fahn and Williams proposed a diagnostic framework
Functional tics share features with primary tic disorders, for psychogenic dystonia, later expanded to all FMD subtypes.74
including sudden onset, distractibility, stereotypy, suggestibility, It classified FMD into four levels of diagnostic certainty: docu-
and fluctuating symptoms.109,112,113 mented FMD, supported by direct evidence (eg, response to sug-
However, they more commonly emerge after age 12, follow- gestion or psychotherapy); clinically established FMD, based on
ing identifiable physical or psychological triggers. Symptoms usu- incongruent signs and psychiatric comorbidities; probable FMD,
ally begin abruptly and are severe at onset. A family history of with suggestive features but lacking definitive evidence; and pos-
tics is typically absent. They are more variable and inconsistent sible FMD, with insufficient positive signs but potential psychiat-
than primary tics, often lacking the rostrocaudal progression or ric associations.22,63,127 This classification was later revised to
waxing-and-waning pattern of Tourette’s syndrome. Additional improve inter-rater reliability. The inclusion of psychiatric symp-
features include entrainment, blocking tics, and exaggerated toms aimed to enhance specificity but had limitations, as these
palilalia, echolalia, or coprolalia-like behaviors.108,109,112–114 features are neither exclusive to FMD nor always present.128
Functional tics frequently co-occur with other FMD, autism These challenges led to a broader reconsideration of diagnostic
spectrum traits, anxiety, or depression. Pharmacological treatments approaches.
for primary tic disorders are often ineffective, while behavioral The most significant paradigm shift emerged with the publica-
therapy and stress management provide better outcomes.108 tion of the Diagnostic and Statistical Manual of Mental Disorders,
Premonitory urge—a subjective sensation preceding tic Fifth Edition (DSM-5), which established positive clinical signs—
execution—was once considered a possible distinguishing such as inconsistency and incongruence—as the cornerstone of
feature.115 However, recent evidence indicates it lacks sufficient diagnosis. The DSM-5 reframed FMD under the umbrella of
diagnostic specificity.116 Functional Neurological Symptom Disorder (Conversion Disorder)
within the Somatic Symptom and Related Disorders category. The
2022 text revision (DSM-5-TR) maintained these criteria.129
Other Forms of Functional Movement The term psychogenic once included somatoform conditions,
factitious disorder, and malingering,8 but these are now recog-
Disorder nized as distinct from FMD. Factitious disorder involves intentional
Beyond common FMD phenotypes, less frequent but clinically symptom production for the sick role, while malingering serves
relevant presentations exhibit hallmark FMD features, including external incentives (eg, financial or legal gain), whereas FMD
variability, inconsistency, and incongruence with known neuro- presents with involuntary symptoms.130,131 Symptom exaggeration
logical patterns. may occur but is not inherent to FMD and is seen in other
Functional chorea involves continuous, flowing, irregular or chronic conditions. Clear differentiation is essential to reduce
non-patterned movements lacking the stereotypy and rhythmicity stigma and ensure appropriate care.
of neurodegenerative chorea.117 Functional hemiballismus presents Accurate FMD diagnosis requires a patient-centered neuropsy-
with abrupt, exaggerated, large-amplitude flinging movements chiatric evaluation.132 Positive signs—variability, distractibility,
without the subthalamic lesion typical of structural cases. Similarly, entrainment, and incongruence—help distinguish FMD from
functional hemifacial spasm causes unilateral facial twitching that mimics, improving accuracy and reducing unnecessary testing
does not follow classic facial nerve pathology.6,118 and hospital visits.133 A structured five-phase diagnostic process
Other forms include functional stomatognathic disorders (jaw has been proposed to guide assessment, enhance communication,
clenching, tongue thrusting),119,120 functional eye movement and support early intervention through multidisciplinary
disorders (irregular gaze shifts, ptosis, eyelid fluttering),121 and collaboration.134,135 This approach ensures timely diagnosis,
functional palatal tremor—rhythmic, soft palate, uvula, or pha- patient validation, and appropriate rehabilitation (Fig. 2).
ryngeal movements, causing a fluttering sensation in the throat
or speech disturbances.122 Functional head tremor and functional
speech or voice disorders—dysphonia or effortful phonation— Phased Diagnostic Process for
also exhibit abrupt onset, distractibility, and fluctuation.123,124
Functional camptocormia, marked by involuntary forward Functional Movement Disorder
trunk flexion, improves when supine—distinguishing it from Phase 1: Clinical History and Symptom
other causes such as parkinsonism or myopathy.125
Assessment
Functional writer’s cramp mimics task-specific dystonia but
lacks consistent activation patterns,126 while functional ataxia A detailed clinical history is essential for diagnosing FMD.
presents with unsteady gait, limb incoordination, or exaggerated Clinicians should assess motor and non-motor symptoms, psychi-
postural sway that improves with distraction.104 atric comorbidities, and systemic complaints, prioritizing the

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REVIEW INSIGHTS INTO FUNCTIONAL MOVEMENT DISORDER.

Figure 2. Stepwise diagnostic approach to functional movement disorder (FMD). This figure outlines a five-phase model for the clinical
evaluation of FMD, integrating neurological examination, psychiatric assessment, diagnostic testing, and patient-centred communication.
The model facilitates timely diagnosis, enhances patient understanding, and supports the development of personalized treatment plans.

8 MOVEMENT DISORDERS CLINICAL PRACTICE 2025. doi: 10.1002/mdc3.70136

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E. ORTEGA-ROBLES ET AL. REVIEW

most disabling symptoms. Key aspects include age and mode of including websites, support groups, and handouts, can facilitate
onset (sudden vs gradual), potential triggers (eg, trauma, illness, patient engagement and support.
surgery), and the pattern of symptom evolution, including fluc-
tuations, variability across settings, and functional impact. Exacer-
bating (eg, stress, fatigue, pain) and relieving (eg, distraction, Phase 5: Follow-Up and Long-Term
relaxation) factors offer diagnostic clues.136 It is also important to Monitoring
explore the patient’s beliefs about symptom origin, perceived
Sustained follow-up is essential to reinforce the diagnosis, moni-
impact, recovery expectations, and past diagnostic experiences,
tor progress, and adjust treatment. Management should begin
including misdiagnosis, medical trauma, or invalidation, which
soon after diagnosis and involve a multidisciplinary team comprising
may influence illness behavior and treatment engagement.
neurologists, physiotherapists, psychologists, and other specialists
trained in functional disorders. Regular visits help identify bar-
riers to recovery and prevent relapse. Reviewing positive signs
Phase 2: Neurological Examination for
and maintaining open, supportive communication is important if
Positive Signs doubts arise. An open-door policy for re-evaluation fosters trust
A focused neurological examination is essential to identify positive and accommodates changing patient perspectives.
signs inconsistent with structural neurological disease. Table 1
summarizes key features. In tremor, entrainment—tremor fre-
quency modulation during contralateral movement—and the
whack-a-mole sign, where tremor shifts to other body parts under Treatment
resistance, support diagnosis. For weakness, Hoover’s sign shows Treatment of FMD has evolved significantly over the past
preserved strength during contralateral hip flexion despite appar- decade, with increasing evidence supporting a multidisciplinary
ent ipsilateral hip extension weakness, and give-way weakness approach that combines physical rehabilitation, psychological
involves abrupt loss of resistance. Gait tests, such as the windmill therapies, neuromodulation, pharmacological interventions, and
sign (flailing arms during retropulsion) and the chair test (ability to digital tools. Analysis of 24 clinical trials conducted since 2015
move a chair despite gait complaints), reveal inconsistency. These demonstrates promising outcomes across a range of modalities.
findings support a rule-in diagnosis of FMD. To aid clinical decision-making, we have synthesized these
results into a structured overview of therapeutic efficacy and fea-
sibility (Supplementary Table S1).
Phase 3: Diagnostic Confirmation and Cognitive behavioral therapy (CBT) is a consistently effective
Exclusion of Other Conditions intervention for FMD. Espay et al56 reported symptom and neu-
FMD is diagnosed clinically using positive signs, but further test- ral activity improvements in functional tremor, while Richardson
ing may be needed to exclude coexisting neurological disease. et al138 found CBT reduced cognitive biases. When combined
Investigations should be guided by phenotype. Symptoms with physiotherapy, it enhances the quality of life.139 A
suggesting motor neuron disease, cerebellar dysfunction, or par- telehealth CBT pilot showed high adherence but no primary
kinsonism may require neuroimaging or laboratory tests.137 outcome changes.140 In children with functional tic-like behav-
Neurophysiological assessments such as surface electromyography iors, psychoeducation groups were beneficial.141 CBT alone or
or tremor analysis can aid diagnosis in selected cases. Lack of with physical activity reduced symptoms,142 and nocebo hypoth-
response to treatments like propranolol for tremor is not diagnos- esis CBT sometimes led to rapid recovery.143
tic, as it can occur in both functional and non-functional disor- Physiotherapy, both in-person and via telemedicine, also plays a
ders. Psychiatric comorbidities—including depression, anxiety, central role in treatment. Nielsen et al144 reported objective
and post-traumatic stress disorder—should be assessed, as they motor improvement following physiotherapy, and Demartini
influence prognosis and treatment, though they are not required et al145 confirmed the feasibility of delivering this treatment
for diagnosis. remotely. However, results from the large Physio4FMD trial rev-
ealed no significant difference between specialist physiotherapy
and standard care, despite subjective reports of benefit, unde-
Phase 4: Diagnostic Communication and rscoring the importance of individualized treatment planning.146
Neuromodulation techniques have shown variable but encourag-
Patient Education
ing outcomes, such as repetitive transcranial magnetic stimulation
Effective, empathetic communication is central to patient under- (rTMS) and intermittent theta burst stimulation (iTBS). Taib
standing and acceptance of the diagnosis. Clinicians should et al147 demonstrated that rTMS improved motor function in
emphasize that the diagnosis is based on objective signs, reinforcing functional tremor, while Park et al148 reported limited efficacy
that symptoms are genuine, involuntary, and treatable. Simple meta- with transcranial direct current stimulation (tDCS) combined
phors, such as comparing FMD to a “software problem,” can aid with yoga. McWhirter et al149 and Garcin et al150 found cortical
understanding. Demonstrating positive signs during the exam modulation effects with TMS, though clinical benefits were less
builds trust and reduces uncertainty. Validated educational resources, pronounced. More recently, Spagnolo et al151 showed that iTBS

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REVIEW INSIGHTS INTO FUNCTIONAL MOVEMENT DISORDER.

targeting corticolimbic networks improved symptom control and Digital and technology-assisted therapies are emerging. Virtual
enhanced functional connectivity. reality (VR)-based interventions, such as mirror visual feedback
Pharmacological treatments have limited evidence. Botulinum and exposure therapy, have shown potential.154 Smartphone-
toxin (BoNT) was no better than placebo in jerky/tremulous based tools offer accessible, low-cost interventions that reinforce
FMD, though placebo effects were notable.152 Similarly, BoNT self-management strategies.155
prior to CBT did not enhance outcomes in functional Evidence supports multidisciplinary treatment, combining physical
dystonia.153 rehabilitation and psychological support. Early trials of

TABLE 2 Therapeutic algorithm for Functional Movement Disorder

Step Key actions Involved specialists

1. Establish diagnosis and engage • Perform a detailed neurological examination, Neurologist, psychiatrist, primary care
the patient identifying positive clinical signs of FMD. physician
• Deliver the diagnosis using a clear, empathetic,
and biopsychosocial explanation.
• Acknowledge and validate the patient’s
symptoms to build trust and promote
engagement.
2. Formulate an integrative • Develop a multimodal management strategy Neurologist, physiotherapist, occupational
treatment plan based on symptom profile and patient goals. therapist, psychotherapist
• Ensure active patient involvement in setting
realistic objectives and therapy priorities.
• Coordinate care across a transdisciplinary team
to support holistic management.
3. Neurology and • Exclude coexisting neurological disorders where Neurologist, rehabilitation physician
neurorehabilitation appropriate.
• Provide psychoeducation on symptom
mechanisms and treatment expectations.
• Prescribe pharmacotherapy if indicated (eg, for
anxiety, depression, or pain).
4. Physiotherapy and occupational • Apply active retraining methods (eg, guided Physiotherapist, occupational therapist
therapy motor control, graded exposure).
• Incorporate attentional modulation strategies
such as distraction and sensory feedback.
• Avoid reinforcing maladaptive behaviors or
excessive focus on symptoms.
5. Psychotherapeutic and • Target maladaptive beliefs, stress response, and Psychotherapist, psychiatrist,
psychosomatic interventions emotion dysregulation. psychosomatic specialist
• Offer CBT, ACT, EMDR, or trauma-focused
modalities as appropriate.
• Support return to work, social reintegration, and
functional recovery.
6. Mind–body and creative • Introduce body awareness and relaxation Mind–body therapist, art therapist,
therapies practices (eg, mindfulness, yoga, Feldenkrais). psychologist
• Use expressive therapies (eg, music, dance, or art
therapy) to support emotional processing.
• Consider adjunct techniques such as biofeedback
or hypnosis for symptom regulation.
7. Ongoing monitoring and • Track clinical response and adjust treatment All disciplines involved in care
adaptation plans accordingly.
• Encourage self-management, coping strategies,
and gradual return to daily activities.
• Provide long-term follow-up and
multidisciplinary support when required.

Abbreviations: ACT, acceptance and commitment therapy; CBT, cognitive behavioral therapy; EMDR, eye movement desensitization and reprocessing.

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E. ORTEGA-ROBLES ET AL. REVIEW

TABLE 3 Prognostic factors associated with recovery in Functional Movement Disorder

Predictors of good prognosis Predictors of poor prognosis

• Patient-perceived control over recovery158 • Older age at diagnosis158

• Early and accurate diagnosis 2
• Strong belief in the permanence of symptoms158
• Younger age at symptom onset2 • Delayed or missed diagnosis2
• Shorter symptom duration 2,159
• Psychiatric comorbidities (eg, anxiety*†, depression*, personality disorders)2,67
• Presence of tremor phenotype 2
• Traumatic or psychological precipitating events2,67
• Belief that treatment is effective 67,159
• Older age at symptom onset2
• Anxiety (in some studies)a,b, 67,159 • High Beck Hopelessness Scale score2
• Reduction or removal of psychosocial stressors 67,159
• Longer symptom duration*2,67,159
• High adherence to treatment 67
• Prominent non-motor symptoms (pain, fatigue*, cognitive dysfunction)2
• Use of specific pharmacological agents 159
• Poor therapeutic alliance or dissatisfaction with healthcare provider67,159
• Good physical health status159 • Negative perception of social support67
• Positive perception of social support 159
• Other negative indicators:67
— Secondary gain
— Neurological or medical comorbidities
— Functional speech involvement
— Family history of neuropsychiatric illness
— Emotional exhaustion or somatization
— Frequent changes in healthcare providers
• Inconsistent motor presentations159
• Active smoking67,159
• High suggestibility159

a
Reported as not significantly associated with outcome in some studies.
b
Findings are inconsistent across studies.

neuromodulation and digital therapies are promising, but further Despite increased interest in outcomes research, the field lacks
research is needed to confirm long-term efficacy and identify suit- standardized, validated tools that reflect the complex and fluctu-
able candidates. A structured therapeutic algorithm is outlined in ating nature of FND.160 Current measures often miss patient-
Table 2.156 centred outcomes, and discrepancies between clinician and
patient reports are common, which may hold clinical signifi-
cance. These limitations hinder cross-study comparisons and may
obscure treatment effects. Outcome measures that are valid, clin-
Prognosis ically relevant, and reflect patient priorities are essential for
FMD prognosis varies widely and is influenced by multiple fac- assessing treatment efficacy and improving long-term outcomes.
tors, including access to appropriate treatment. Without targeted
intervention, outcomes are generally poor. In an eight-year
follow-up study (n = 23), 82.6% of patients had persistent dis-
abling symptoms,157 and another study reported symptom persis-
Conclusion
tence in up to 90% after 3.2 years.23 FMD is a complex disorder involving neurological, psychologi-
Treatment-based studies offer more favorable outcomes. Fac- cal, and social factors. Despite advances in neuroimaging and
tor et al8 reported symptom resolution in 35% of patients at neurophysiology, diagnosis remains clinical, based on positive
2 years, while Williams et al62 found a 25% resolution rate. In a signs.2 The condition’s heterogeneity calls for personalized treat-
larger cohort (n = 346), Thomas and Jankovic observed ment that considers symptom profile, cognitive style, com-
improvement in 42.4% over 8 years, while 21.2% worsened and orbidities, and functional goals. Multidisciplinary approaches
15.2% remained unchanged.11 integrating neurological, psychological, and rehabilitative care
Data from the Physio4FMD trial provide insights into predictors offer the best outcomes.
of recovery. A secondary analysis by Nielsen et al158 showed that CBT is a key treatment supported by strong evidence for
older age and strong beliefs in symptom permanence predicted improving symptoms.56,138 Its success relies on addressing mal-
poorer outcomes, while a greater sense of control was linked to adaptive beliefs through tailored approaches. Physiotherapy is
improvement. Symptom duration, fatigue, pain, and psychiatric also effective, especially when combined with psychological care.
comorbidities did not significantly influence treatment response. Remote delivery is feasible but requires appropriate patient selec-
Table 3 summarizes clinical predictors of recovery, which can tion and engagement.146,161
aid in diagnostic feedback, managing expectations, and treatment Neuromodulation techniques (rTMS, iTBS, tDCS) have
planning.2,67,158,159 shown inconsistent results, although individualizing stimulation

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REVIEW INSIGHTS INTO FUNCTIONAL MOVEMENT DISORDER.

parameters and targeting relevant brain networks may this work. The authors confirm that patient consent was not
enhance efficacy. required for this work. We confirm that we have read the
Digital therapies—including VR-based,154 apps,155 and Journal’s position on issues involved in ethical publication and
telehealth140,145—expand access and offer innovative, scalable affirm that this work is consistent with those guidelines.
solutions, but must be adapted to patient’s cognitive and emo- Funding Sources and Conflict of Interest: No specific
tional needs while maintaining therapeutic connection. funding was received for this work. The authors declare no con-
Patient empowerment is essential. Perceived control over flicts of interest relevant to this work.
symptoms strongly predicts outcomes,158 highlighting the value Financial Disclosures for the previous 12 months: The
of education, shared decision-making, and collaborative goals. authors declare no additional disclosures to report.
Success depends on both treatment choice and its delivery. Clear,
empathetic communication improves outcomes, while poor
explanation and dismissive language worsen them.35,162–164 Data Availability Statement
Framing symptoms as involuntary and treatable within a biopsy- Data sharing is not applicable to this article as no new data were
chosocial model promotes engagement and facilitates recovery. created or analyzed in this study. ■
Despite progress, no validated biomarkers exist for diagnosis
or treatment monitoring. Although neuroimaging and electro-
physiology have revealed network-level changes, none are suit-
able for clinical use.59 Biomarker development could improve
diagnosis, prognosis, and personalized care.
References
1. Edwards MJ, Bhatia KP. Functional (psychogenic) movement disorders:
The limitations of this review must be acknowledged. Despite merging mind and brain. Lancet Neurol 2012;11(3):250–260.
using a structured search strategy, the final study selection was 2. Park JE. Functional movement disorders: updates and clinical overview.
guided by the authors’ discretion, introducing potential bias. We J Mov Disord 2024;17(3):251–261.
did not conduct formal quality assessments or statistical pooling, 3. Schrag A, Lang AE. Psychogenic movement disorders. Curr Opin Neurol
2005;18(4):399–404.
limiting our ability to assess consistency or quantify effect sizes.
4. DeJong RN. Abnormal movements. The Neurologic Examination: Incor-
Inherent to narrative reviews, these constraints should be consid- porating the Fundamentals of Neuroanatomy and Neurophysiology. 2nd ed.
ered when interpreting our conclusions. New York: Hoeber-Harper; 1958:521–523.
In summary, improving outcomes in FMD requires an inte- 5. Fahn S. Psychogenic movement disorders. In: Marsden CD, Fahn S,
eds. Movement disorders. Cambridge: Butterworth-Heinemann; 1994:
grated, patient-centred approach that combines scientific precision 359–372.
with compassionate care. Priorities for future research include bio- 6. Ertan S, Uluduz D, Ozekmekçi S, et al. Clinical characteristics of
marker development, validated outcome measures, and adaptive, 49 patients with psychogenic movement disorders in a tertiary clinic in
Turkey. Mov Disord 2009;24(5):759–762.
individualized treatments through multidisciplinary collaboration.
7. Stone J, Carson A, Duncan R, et al. Who is referred to neurology
clinics?--the diagnoses made in 3781 new patients. Clin Neurol Neuro-
surg 2010;112(9):747–751.
8. Factor SA, Podskalny GD, Molho ES. Psychogenic movement disor-
Author Roles ders: frequency, clinical profile, and characteristics. J Neurol Neurosurg
Psychiatry 1995;59(4):406–412.
(1) Research project: A. Conception, B. Organization, 9. Park JE. Clinical characteristics of functional movement disorders: a
clinic-based study. Tremor Other Hyperkinet Mov (N Y) 2018;8:504.
C. Execution; (2) Statistical Analysis: A. Design, B. Execution,
10. Portera-Cailliau C, Victor D, Frucht S, Fahn S. Movement disorders
C. Review and Critique; (3) Manuscript Preparation: A. Writing fellowship training program at Columbia University medical center in
of the first draft, B. Review and Critique. 2001-2002. Mov Disord 2006;21(4):479–485.
E.O.-R.: 1B, 1C, 3A, 3B. 11. Thomas M, Jankovic J. Psychogenic movement disorders: diagnosis and
management. CNS Drugs 2004;18(7):437–452.
A.S.: 1C, 3B.
12. Ramsay N, Stone J, Fadiloglu K, et al. Functional neurological disorder:
J.R.-B.: 1C, 3B. a common reason for a neurology inpatient referral. Eur J Neurol 2023;
O.A.-C.: 1A, 1B, 1C, 3A, 3B. 30(12):3886–3889.
13. Kletenik I, Sillau SH, Isfahani SA, LaFaver K, Hallett M, Berman BD.
Gender as a risk Factor for functional movement disorders: the role of
sexual abuse. Mov Disord Clin Pract 2020;7(2):177–181.

Acknowledgments 14. Lidstone SC, Costa-Parke M, Robinson EJ, Ercoli T, Stone J. Func-
tional movement disorder gender, age and phenotype study: a system-
atic review and individual patient meta-analysis of 4905 cases. J Neurol
We thank all those who have made us better—friends, foes, and Neurosurg Psychiatry 2022;93(6):609–616.
those who said nothing. 15. Cubo E, Hinson VK, Goetz CG, et al. Transcultural comparison of
psychogenic movement disorders. Mov Disord 2005;20(10):1343–1345.
16. Munhoz RP, Zavala JA, Becker N, Teive HA. Cross-cultural influences
on psychogenic movement disorders - a comparative review with a
Brazilian series of 83 cases. Clin Neurol Neurosurg 2011;113(2):115–118.
Disclosures 17. Harris SR. Psychogenic movement disorders in children and adoles-
cents: an update. Eur J Pediatr 2019;178(4):581–585.
Ethical Compliance Statement: The authors confirm that the 18. Ferrara J, Jankovic J. Psychogenic movement disorders in children. Mov
approval of an institutional review board was not required for Disord 2008;23(13):1875–1881.

12 MOVEMENT DISORDERS CLINICAL PRACTICE 2025. doi: 10.1002/mdc3.70136

 23301619, 0, Downloaded from [Link] by Egyptian National Sti. Network (Enstinet), Wiley Online Library on [19/05/2025]. See the Terms and Conditions ([Link] on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
E. ORTEGA-ROBLES ET AL. REVIEW

19. Schwingenschuh P, Pont-Sunyer C, Surtees R, Edwards MJ, Bhatia KP. 44. van Wouwe NC, Mohanty D, Lingaiah A, Wylie SA, LaFaver K.
Psychogenic movement disorders in children: a report of 15 cases and a Impaired action control in patients with functional movement disorders.
review of the literature. Mov Disord 2008;23(13):1882–1888. J Neuropsychiatry Clin Neurosci 2020;32(1):73–78.
20. Chouksey A, Pandey S. Functional movement disorders in elderly. 45. Lin D, Castro P, Edwards A, et al. Dissociated motor learning and de-
Tremor Other Hyperkinet Mov (N Y) 2019;9:1–6. adaptation in patients with functional gait disorders. Brain 2020;143(8):
2594–2606.
21. Hinson VK, Haren WB. Psychogenic movement disorders. Lancet Neu-
rol 2006;5(8):695–700. 46. Maurer CW, Liu VD, LaFaver K, et al. Impaired resting vagal tone in
patients with functional movement disorders. Parkinsonism Relat Disord
22. Ranawaya R, Riley D, Lang A. Psychogenic dyskinesias in patients
2016;30:18–22.
with organic movement disorders. Mov Disord 1990;5(2):127–133.
47. Aybek S, Nicholson TR, O’Daly O, Zelaya F, Kanaan RA, David AS.
23. Feinstein A, Stergiopoulos V, Fine J, Lang AE. Psychiatric outcome in
Emotion-motion interactions in conversion disorder: an FMRI study.
patients with a psychogenic movement disorder: a prospective study.
PLoS One 2015;10(4):e0123273.
Neuropsychiatry Neuropsychol Behav Neurol 2001;14(3):169–176.
48. Vyas A, Jadhav S, Chattarji S. Prolonged behavioral stress enhances syn-
24. Ludwig L, Pasman JA, Nicholson T, et al. Stressful life events and mal-
aptic connectivity in the basolateral amygdala. Neuroscience 2006;143(2):
treatment in conversion (functional neurological) disorder: systematic
387–393.
review and meta-analysis of case-control studies. Lancet Psychiatry 2018;
5(4):307–320. 49. Mitra R, Sapolsky RM. Acute corticosterone treatment is sufficient to
induce anxiety and amygdaloid dendritic hypertrophy. Proc Natl Acad
25. Kranick S, Ekanayake V, Martinez V, Ameli R, Hallett M, Voon V.
Sci U S A 2008;105(14):5573–5578.
Psychopathology and psychogenic movement disorders. Mov Disord
2011;26(10):1844–1850. 50. Castillo-G
omez E, Pérez-Rando M, Bellés M, et al. Early social isola-
tion stress and perinatal NMDA receptor antagonist treatment induce
26. Hull M, Parnes M, Jankovic J. Increased incidence of functional (psy-
changes in the structure and neurochemistry of inhibitory neurons of
chogenic) movement disorders in children and adults amid the
the adult amygdala and prefrontal cortex. eNeuro 2017;4(2):1–23.
COVID-19 pandemic: a cross-sectional study. Neurol Clin Pract 2021;
11(5):e686–e690. 51. Ohta KI, Suzuki S, Warita K, et al. The effects of early life stress on the
excitatory/inhibitory balance of the medial prefrontal cortex. Behav
27. Mostile G, Geroin C, Erro R, et al. Data-driven clustering of combined
Brain Res 2020;379:112306.
functional motor disorders based on the Italian registry. Front Neurol
2022;13:987593. 52. Voon V, Brezing C, Gallea C, et al. Emotional stimuli and motor con-
version disorder. Brain 2010;133(Pt 5):1526–1536.
28. Tinazzi M, Geroin C, Marcuzzo E, et al. Functional motor phenotypes:
to lump or to split? J Neurol 2021;268(12):4737–4743. 53. Hassa T, Sebastian A, Liepert J, Weiller C, Schmidt R, Tüscher O.
Symptom-specific amygdala hyperactivity modulates motor control net-
29. Tomi
c A, Ječmenica Luki
c M, Petrovi
c I, et al. Changes of phenotypic
work in conversion disorder. Neuroimage Clin 2017;15:143–150.
pattern in functional movement disorders: a prospective cohort study.
Front Neurol 2020;11:582215. 54. Piramide N, Sarasso E, Tomic A, et al. Functional MRI connectivity of
the primary motor cortex in functional dystonia patients. J Neurol 2022;
30. Gilmour GS, Langer LK, Lang AE, MacGillivray L, Lidstone SC. Neu-
269(6):2961–2971.
ropsychiatric phenotypes in functional movement disorder. CNS Spectr
2023;28(6):747–755. 55. Sojka P, Loš
ak J, Lamoš M, et al. Processing of emotions in functional
movement disorder: an exploratory fMRI study. Front Neurol 2019;10:861.
31. Demartini B, Nisticò V, Edwards MJ, Gambini O, Priori A. The patho-
physiology of functional movement disorders. Neurosci Biobehav Rev 56. Espay AJ, Ries S, Maloney T, et al. Clinical and neural responses to
2021;120:387–400. cognitive behavioral therapy for functional tremor. Neurology 2019;
93(19):e1787–e1798.
32. Hallett M. Functional Neurologic Disorder, La Lésion Dynamique:
2024 Wartenberg Lecture. Neurology 2024;103(11):e210051. 57. Faul L, Knight LK, Espay AJ, Depue BE, LaFaver K. Neural activity in
functional movement disorders after inpatient rehabilitation. Psychiatry
33. Saxena A, Godena E, Maggio J, Perez DL. Towards an outpatient
Res Neuroimaging 2020;303:111125.
model of Care for Motor Functional Neurological Disorders: a neuro-
psychiatric perspective. Neuropsychiatr Dis Treat 2020;16:2119–2134. 58. Bègue I, Adams C, Stone J, Perez DL. Structural alterations in func-
tional neurological disorder and related conditions: a software and hard-
34. Baizabal-Carvallo JF, Hallett M, Jankovic J. Pathogenesis and patho-
ware problem? Neuroimage Clin 2019;22:101798.
physiology of functional (psychogenic) movement disorders. Neurobiol
Dis 2019;127:32–44. 59. Perez DL, Nicholson TR, Asadi-Pooya AA, et al. Neuroimaging in
functional neurological disorder: state of the field and research agenda.
35. Hallett M, Aybek S, Dworetzky BA, McWhirter L, Staab JP, Stone J.
Neuroimage Clin 2021;30:102623.
Functional neurological disorder: new subtypes and shared mechanisms.
Lancet Neurol 2022;21(6):537–550. 60. Diez I, Williams B, Kubicki MR, Makris N, Perez DL. Reduced limbic
microstructural integrity in functional neurological disorder. Psychol Med
36. Drane DL, Fani N, Hallett M, Khalsa SS, Perez DL, Roberts NA. A
2021;51(3):485–493.
framework for understanding the pathophysiology of functional neuro-
logical disorder. CNS Spectr 2020;26:555–561. 61. Tinazzi M, Morgante F, Marcuzzo E, et al. Clinical correlates of func-
tional motor disorders: an Italian multicenter study. Mov Disord Clin
37. Sasikumar S, Strafella AP. The neuroimaging evidence of brain abnormal-
Pract 2020;7(8):920–929.
ities in functional movement disorders. Brain 2021;144(8):2278–2283.
62. Williams DT, Ford B, Fahn S. Phenomenology and psychopathology
38. Sadnicka A, Daum C, Meppelink AM, Manohar S, Edwards M.
related to psychogenic movement disorders. Adv Neurol 1995;65:
Reduced drift rate: a biomarker of impaired information processing in
231–257.
functional movement disorders. Brain 2020;143(2):674–683.
63. Koller W, Lang A, Vetere-Overfield B, et al. Psychogenic tremors.
39. Morgante F, Matinella A, Andrenelli E, et al. Pain processing in func-
Neurology 1989;39(8):1094–1099.
tional and idiopathic dystonia: an exploratory study. Mov Disord 2018;
33(8):1340–1348. 64. Deuschl G, Köster B, Lücking CH, Scheidt C. Diagnostic and patho-
physiological aspects of psychogenic tremors. Mov Disord 1998;13(2):
40. Perez DL, Edwards MJ, Nielsen G, Kozlowska K, Hallett M, LaFrance WC
294–302.
Jr. Decade of progress in motor functional neurological disorder: continuing
the momentum. J Neurol Neurosurg Psychiatry 2021;92:668–677. 65. Bhatia KP, Schneider SA. Psychogenic tremor and related disorders.
J Neurol 2007;254(5):569–574.
41. Huys AML, Bhatia KP, Edwards MJ, Haggard P. The Flip side of
distractibility-executive dysfunction in functional movement disorders. 66. McKeon A, Ahlskog JE, Bower JH, Josephs KA, Matsumoto JY. Psy-
Front Neurol 2020;11(969):969. chogenic tremor: long-term prognosis in patients with electrophysiolog-
ically confirmed disease. Mov Disord 2009;24(1):72–76.
42. Teodoro T, Koreki A, Meppelink AM, et al. Contingent negative vari-
ation: a biomarker of abnormal attention in functional movement disor- 67. Jankovic J, Vuong KD, Thomas M. Psychogenic tremor: long-term
ders. Eur J Neurol 2020;27(6):985–994. outcome. CNS Spectr 2006;11(7):501–508.
43. Marotta A, Fiorio M, Riello M, Demartini B, Tecilla G, Dallocchio C, 68. Kim YJ, Pakiam AS, Lang AE. Historical and clinical features of psy-
Tinazzi M. Attentional avoidance of emotions in functional movement chogenic tremor: a review of 70 cases. Can J Neurol Sci 1999;26(3):
disorders. J Psychosom Res 2020;133:110100. 190–195.

MOVEMENT DISORDERS CLINICAL PRACTICE 2025. doi: 10.1002/mdc3.70136 13

 23301619, 0, Downloaded from [Link] by Egyptian National Sti. Network (Enstinet), Wiley Online Library on [19/05/2025]. See the Terms and Conditions ([Link] on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
REVIEW INSIGHTS INTO FUNCTIONAL MOVEMENT DISORDER.

69. Piboolnurak P, Rothey N, Ahmed A, Ford B, Yu Q, Xu D, 97. Keane JR. Hysterical gait disorders: 60 cases. Neurology 1989;39(4):586–589.
Pullman SL. Psychogenic tremor disorders identified using tree-based
98. Baik JS, Lang AE. Gait abnormalities in psychogenic movement disor-
statistical algorithms and quantitative tremor analysis. Mov Disord 2005;
ders. Mov Disord 2007;22(3):395–399.
20(12):1543–1549.
99. Hayes MW, Graham S, Heldorf P, de Moore G, Morris JG. A video
70. Gironell A, L
opez-Villegas D, Barbanoj M, Kulisevsky J. Psychogenic
review of the diagnosis of psychogenic gait: appendix and commentary.
tremor: clinical, electrophysiologic and psychopathologic assessment.
Mov Disord 1999;14(6):914–921.
Neurologia 1997;12(7):293–299.
100. Lempert T, Brandt T, Dieterich M, Huppert D. How to identify psy-
71. O’Suilleabhain PE, Matsumoto JY. Time-frequency analysis of tremors.
chogenic disorders of stance and gait. A video study in 37 patients.
Brain 1998;121(Pt 11):2127–2134.
J Neurol 1991;238(3):140–146.
72. Raethjen J, Kopper F, Govindan RB, Volkmann J, Deuschl G. Two
101. Diukova GM, Stoliarova AV. Psychogenic disorders of stance and gait
different pathogenetic mechanisms in psychogenic tremor. Neurology
as seen in videotaping. Zh Nevrol Psikhiatr Im S S Korsakova 2001;
2004;63(5):812–815.
101(12):13–18.
73. Fahn S, Williams D, Reches A, Lesser RP, Jankovic J, Silberstein S.
102. Woolley SM, Rubin AM, Chronis CB, Dailey V, Bork CE, Gerard G.
Hysterical dystonia, a rare disorder: report of five documented cases.
Static stabilometry, transcranial doppler, and single photon emission
Neurology 1983;33(Suppl 2):161.
computed tomography in patients with central dizziness. Am J Otol
74. Fahn S, Williams DT. Psychogenic dystonia. Adv Neurol 1988;50:431–455. 1994;15(6):739–747.
75. Scott BL. Evaluation and treatment of dystonia. South Med J 2000;93(8): 103. Allum JH, Shepard NT. An overview of the clinical use of dynamic
746–751. posturography in the differential diagnosis of balance disorders. J Vestib
Res 1999;9(4):223–252.
76. Ferraz HB, Andrade LA. Symptomatic dystonia: clinical profile of
46 Brazilian patients. Can J Neurol Sci 1992;19(4):504–507. 104. Manto MU. Discrepancy between dysmetric centrifugal movements
and normometric centripetal movements in psychogenic ataxia. Eur
77. Lang AE. Psychogenic dystonia: a review of 18 cases. Can J Neurol Sci
Neurol 2001;45(4):261–265.
1995;22(2):136–143.
105. Nilles C, Pringsheim TM, Martino D. The recent surge of functional
78. Schmidt S, Wisser R, Heitmann R. Psychosomatic aspects of focal dys-
movement disorders: social distress or greater awareness? Curr Opin Neu-
tonia: two case reports. Psychother Psychosom 1994;44(7):247–250.
rol 2022;35(4):485–493.
79. Vargas AP, Carod-Artal FJ, Del Negro MC, Rodrigues MP. Psycho-
106. Cavanna AE, Purpura G, Riva A, Nacinovich R, Seri S. New-onset
genic dystonia: report of 2 cases. Arq Neuropsiquiatr 2000;58(2b):
functional tics during the COVID-19 pandemic: clinical characteristics
522–530.
of 105 cases from a single centre. Eur J Neurol 2023;30(8):2411–2417.
80. Kaneko K. A patient with diagnosis of schizophrenia and psychogenic
107. Pringsheim T, Ganos C, McGuire JF, et al. Rapid onset functional tic-
torticollis. Assistance of the patient and her family. Significance of case
like behaviors in young females during the COVID-19 pandemic. Mov
studies in teaching the technics in psychological support of patients.
Disord 2021;36(12):2707–2713.
Hokenfu Zasshi 1987;43(10):906–919.
108. Periš A, Telarovi
c S. On differences between Gilles de la Tourette syn-
81. Tijssen MA, Marsden JF, Brown P. Frequency analysis of EMG activity
drome and psychogenic/functional tics: a narrative review. Psychiatr
in patients with idiopathic torticollis. Brain 2000;123(Pt 4):677–686.
Danub 2019;31(Suppl 5):732–736.
82. Espay AJ, Morgante F, Purzner J, Gunraj CA, Lang AE, Chen R. Cor-
109. Baizabal-Carvallo JF, Jankovic J. The clinical features of psychogenic
tical and spinal abnormalities in psychogenic dystonia. Ann Neurol 2006;
movement disorders resembling tics. J Neurol Neurosurg Psychiatry 2014;
59(5):825–834.
85(5):573–575.
83. Monday K, Jankovic J. Psychogenic myoclonus. Neurology 1993;43(2):
110. Lang AE. General overview of psychogenic movement disorders: epide-
349–352.
miology, diagnosis, and prognosis. In: Hallett M, Fahn S, Jankovic J,
84. van der Salm SM, Koelman JH, Henneke S, van Rootselaar AF, Lang AE, Cloninger CR, Yudofsky SC, eds. Psychogenic Movement Disor-
Tijssen MA. Axial jerks: a clinical spectrum ranging from propriospinal ders Neurology and Neuropsychiatry. Philadelphia, PA: Lippincott Wil-
to psychogenic myoclonus. J Neurol 2010;257(8):1349–1355. liams & Wilkins; 2006:35–41.
85. Brown P, Thompson PD. Electrophysiological aids to the diagnosis of 111. Cavanna AE, Spini L, Ferrari S, Purpura G, Riva A, Nacinovich R,
psychogenic jerks, spasms, and tremor. Mov Disord 2001;16(4):595–599. Seri S. Functional tic-like behaviors: from the COVID-19 pandemic to
the Post-pandemic era. Healthcare (Basel) 2024;12(11):1106.
86. Kamble N, Pal PK. Electrophysiology in functional movement disor-
ders: an update. Tremor Other Hyperkinet Mov (N Y) 2023;13:49. 112. Cavanna AE, Purpura G, Riva A, Nacinovich R, Seri S. Functional tics:
expanding the phenotypes of functional movement disorders? Eur J
87. van der Salm SM, Tijssen MA, Koelman JH, van Rootselaar AF. The
Neurol 2023;30(10):3353–3356.
bereitschaftspotential in jerky movement disorders. J Neurol Neurosurg
Psychiatry 2012;83(12):1162–1167. 113. Demartini B, Ricciardi L, Parees I, Ganos C, Bhatia KP, Edwards MJ.
A positive diagnosis of functional (psychogenic) tics. Eur J Neurol 2015;
88. van der Salm SM, Erro R, Cordivari C, et al. Propriospinal myoclonus:
22(3):527.e36.
clinical reappraisal and review of literature. Neurology 2014;83(20):
1862–1870. 114. Maxwell A, Zouki JJ, Eapen V. Integrated cognitive behavioral inter-
vention for functional tics (I-CBiT): case reports and treatment formu-
89. Ugawa Y. How to use clinical neurophysiology in functional neurolog-
lation. Front Pediatr 2023;11:1265123.
ical disorders (FND)? Rinsho Shinkeigaku 2025;65(1):1–7.
115. Amorelli G, Martino D, Pringsheim T. Rapid onset functional tic-like
90. Walters AS, Boudwin J, Wright D, Jones K. Three hysterical move-
disorder outbreak: a challenging differential diagnosis in the COVID-19
ment disorders. Psychol Rep 1988;62(3):979–985.
pandemic. J Can Acad Child Adolesc Psychiatry 2022;31(3):144–151.
91. Lang AE, Koller WC, Fahn S. Psychogenic parkinsonism. Arch Neurol
116. Szejko N, Fletcher J, Martino D, Pringsheim T. Premonitory urge in
1995;52(8):802–810.
patients with tics and functional tic-like behaviors. Mov Disord Clin Pract
92. LaFaver K, Espay AJ. Diagnosis and treatment of functional (psycho- 2024;11(3):276–281.
genic) parkinsonism. Semin Neurol 2017;37(2):228–232.
117. Wischnewski J. Choreatic movement disorders as a psychosomatic syn-
93. Jennings DL, Seibyl JP, Oakes D, Eberly S, Murphy J, Marek K. (123I) drome. Z Psychosom Med Psychoanal 1978;24(1):87–89.
beta-CIT and single-photon emission computed tomographic imaging
118. Tan EK, Jankovic J. Psychogenic hemifacial spasm. J Neuropsychiatry
vs clinical evaluation in parkinsonian syndrome: unmasking an early
Clin Neurosci 2001;13(3):380–384.
diagnosis. Arch Neurol 2004;61(8):1224–1229.
119. Yoshida K. Movement disorders of the stomatognathic system: a blind
94. Tolosa E, Coelho M, Gallardo M. DAT imaging in drug-induced and
spot between dentistry and medicine. Dent Med Probl 2024;61(4):613–625.
psychogenic parkinsonism. Mov Disord 2003;18(Suppl 7):S28–S33.
120. Ho TC, Couch SM, Custer PL. Psychogenic Ptosis. Ophthalmic Plast
95. Gaig C, Martí MJ, Tolosa E, Valldeoriola F, Paredes P, Lomeña FJ,
Reconstr Surg 2022;38(5):448–451.
Nakamae F. 123I-Ioflupane SPECT in the diagnosis of suspected psy-
chogenic parkinsonism. Mov Disord 2006;21(11):1994–1998. 121. Certo F, Salvucci G, Casellato C, Gambini C, Oggioni GD, Bocci T,
Priori A. Non-nystagmus hyperkinetic eye movement disorders. Neurol
96. Rubino FA. Gait disorders. Neurologist 2002;8(4):254–262.
Sci 2025. [Link]

14 MOVEMENT DISORDERS CLINICAL PRACTICE 2025. doi: 10.1002/mdc3.70136

 23301619, 0, Downloaded from [Link] by Egyptian National Sti. Network (Enstinet), Wiley Online Library on [19/05/2025]. See the Terms and Conditions ([Link] on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
E. ORTEGA-ROBLES ET AL. REVIEW

122. Stamelou M, Saifee TA, Edwards MJ, Bhatia KP. Psychogenic palatal a pragmatic, multicentre, phase 3 randomised controlled trial. Lancet
tremor may be underrecognized: reappraisal of a large series of cases. Neurol 2024;23(7):675–686.
Mov Disord 2012;27(9):1164–1168.
147. Taib S, Ory-Magne F, Brefel-Courbon C, Moreau Y, Thalamas C,
123. Ramos VF, Hallett M. Head accelerometry may be useful as a test of Arbus C, Simonetta-Moreau M. Repetitive transcranial magnetic stimu-
psychogenic head tremor. Mov Disord Clin Pract 2014;1(4):395–396. lation for functional tremor: a randomized, double-blind, controlled
study. Mov Disord 2019;34(8):1210–1219.
124. Tezcaner Z, Gökmen MF, Yıldırım S, Dursun G. Clinical features of
psychogenic voice disorder and the efficiency of voice therapy and psy- 148. Park JE, Hong JY, Lee SY. Transcranial direct current stimulation and
chological evaluation. J Voice 2019;33(2):250–254. yoga for functional movement disorders. Neurologist 2021;26(6):
231–236.
125. Skidmore F, Anderson K, Fram D, Weiner W. Psychogenic camp-
tocormia. Mov Disord 2007;22(13):1974–1975. 149. McWhirter L, Ludwig L, Carson A, McIntosh RD, Stone J. Trans-
cranial magnetic stimulation as a treatment for functional (psychogenic)
126. Dauner I, Remschmidt H. Symptom choice and symptom change in a
upper limb weakness. J Psychosom Res 2016;89:102–106.
case of psychogenic writer’s cramp. Prax Kinderpsychol Kinderpsychiatr
1970;19(7):246–252. 150. Garcin B, Mesrati F, Hubsch C, et al. Impact of transcranial magnetic
stimulation on functional movement disorders: cortical modulation or a
127. Shill H, Gerber P. Evaluation of clinical diagnostic criteria for psycho-
behavioral effect? Front Neurol 2017;8:338.
genic movement disorders. Mov Disord 2006;21(8):1163–1168.
151. Spagnolo PA, Parker J, Horovitz S, Hallett M. Corticolimbic modula-
128. Espay AJ, Lang AE. Phenotype-specific diagnosis of functional (psycho-
tion via intermittent theta burst stimulation as a novel treatment for
genic) movement disorders. Curr Neurol Neurosci Rep 2015;15(6):32.
functional movement disorder: a proof-of-concept study. Brain Sci
129. American Psychiatric Association. Diagnostic and Statistical Manual of 2021;11(6):791.
Mental Disorders. Text Revision (DSM-5-TR). 5th ed. Washington,
152. Dreissen YEM, Dijk JM, Gelauff JM, et al. Botulinum neurotoxin
DC: American Psychiatric Association; 2022.
treatment in jerky and tremulous functional movement disorders: a
130. Bass C, Halligan P. Factitious disorders and malingering in relation to func- double-blind, randomised placebo-controlled trial with an open-label
tional neurologic disorders. Handb Clin Neurol 2016;139:509–520, Elsevier. extension. J Neurol Neurosurg Psychiatry 2019;90(11):1244–1250.
131. Edwards MJ, Yogarajah M, Stone J. Why functional neurological disor- 153. Vizcarra JA, Lopez-Castellanos JR, Dwivedi AK, Schmerler DA,
der is not feigning or malingering. Nat Rev Neurol 2023;19(4):246–256. Ries S, Espay AJ. OnabotulinumtoxinA and cognitive behavioral ther-
apy in functional dystonia: a pilot randomized clinical trial. Parkinsonism
132. Reich SG. Psychogenic movement disorders. Semin Neurol 2006;26(3):
Relat Disord 2019;63:174–178.
289–296.
154. Bullock K, Won AS, Bailenson J, Friedman R. Virtual reality-delivered
133. Tinazzi M, Gandolfi M, Menaspà Z, Sandri A, Landi S, Leardini C.
Mirror visual feedback and exposure therapy for FND: a midpoint
Reducing healthcare costs by timely diagnosis and management in func-
report of a randomized controlled feasibility study. J Neuropsychiatry Clin
tional motor disorders. Neurol Sci 2025;46(3):1191–1200.
Neurosci 2020;32(1):90–94.
134. Weissbach A, Bolte C, Münchau A. Conclusion instead of exclusion-
155. Garris JF, Bauman G, Espay AJ. Development and pilot testing of the
the clinical diagnosis of functional movement disorders. Nervenarzt
tremor Retrainer smartphone application for the treatment of functional
2024;95(6):507–515.
tremor. Tremor Other Hyperkinet Mov (N Y) 2023;13:45.
135. Gilmour GS, Lidstone SC. Moving beyond movement: diagnosing
156. Hausteiner-Wiehle C, Schmidt R. Transdisciplinary treatment of func-
functional movement disorder. Semin Neurol 2023;43(1):106–122.
tional movement disorders: integration instead of dissociation.
136. Lagrand TJ, Gelauff JM, Brusse-Keizer M, Lehn AC, Tijssen MAJ. Pos- Nervenarzt 2024;95(6):532–538.
itive signs from the history as an aid for early diagnosis in functional
157. Miyasaki JM, Sa DS, Galvez-Jimenez N, Lang AE. Psychogenic move-
movement disorders: the prospective TASMAN study. Eur J Neurol
ment disorders. Can J Neurol Sci 2003;30(Suppl 1):S94–S100.
2025;32(1):e16525.
158. Nielsen G, Lee TC, Marston L, et al. Which factors predict outcome
137. Anderson KE. Evaluation and diagnosis of psychogenic disorders in
from specialist physiotherapy for functional motor disorder? Prognostic
neurological patients. Semin Neurol 2006;26(3):283–288.
modelling of the Physio4FMD intervention. J Psychosom Res 2025;190:
138. Richardson M, Kleinstäuber M, Wong D. Nocebo-hypothesis cogni- 112056.
tive behavioral therapy (NH-CBT) for persons with functional neuro-
159. Thomas M, Vuong KD, Jankovic J. Long-term prognosis of patients
logical symptoms (motor type): design and implementation of a
with psychogenic movement disorders. Parkinsonism Relat Disord 2006;
randomized active-controlled trial. Front Neurol 2020;11:586359.
12(6):382–387.
139. Macías-García D, Méndez-Del Barrio M, Canal-Rivero M, et al. Com-
160. Nicholson TR, Carson A, Edwards MJ, et al. Outcome measures for
bined physiotherapy and cognitive behavioral therapy for functional
functional neurological disorder: a review of the theoretical complexi-
movement disorders: a randomized clinical trial. JAMA Neurol 2024;
ties. J Neuropsychiatry Clin Neurosci 2020;32(1):33–42.
81(9):966–976.
161. Nielsen G, Stone J, Buszewicz M, et al. Physio4FMD: protocol for a
140. Kulikov VN, Gillett DA, Maurer CW. A pilot group cognitive behav-
multicentre randomised controlled trial of specialist physiotherapy for
ioral therapy telehealth intervention for functional movement disorder.
functional motor disorder. BMC Neurol 2019;19(1):242.
Mov Disord 2024;39(12):2298–2300.
162. Gelauff JM, Dreissen YE, Tijssen MA, Stone J. Treatment of functional
141. Duncan M, Pearman Z, Harrold K, et al. Evaluation of a psycho-
motor disorders. Curr Treat Options Neurol 2014;16(4):286.
education group for children presenting with functional tic-like behav-
iours. Clin Child Psychol Psychiatry 2024;29(3):1011–1025. 163. Zeun D, Hunter H. Physiotherapy management of functional move-
ment disorders: the patient perspective. Disabil Rehabil 2024;46(19):
142. Dallocchio C, Tinazzi M, Bombieri F, Arn
o N, Erro R. Cognitive
4359–4367.
Behavioural therapy and adjunctive physical activity for functional
movement disorders (conversion disorder): a pilot, single-blinded, ran- 164. Gelauff J, Stone J, Edwards M, Carson A. The prognosis of functional
domized study. Psychother Psychosom 2016;85(6):381–383. (psychogenic) motor symptoms: a systematic review. J Neurol Neurosurg
Psychiatry 2014;85(2):220–226.
143. Richardson MB. Nocebo Hypothesis Cognitive Behavioural Therapy
(NH-CBT) for the treatment of functional neurological symptom disor-
der: University of Otago; 2024.
144. Nielsen G, Buszewicz M, Stevenson F, et al. Randomised feasibility
study of physiotherapy for patients with functional motor symptoms.
J Neurol Neurosurg Psychiatry 2017;88(6):484–490.
Supporting Information
145. Demartini B, Bombieri F, Goeta D, Gambini O, Ricciardi L, Tinazzi M. Supporting information may be found in the online version of
A physical therapy programme for functional motor symptoms: a tele-
medicine pilot study. Parkinsonism Relat Disord 2020;76:108–111.
this article.
146. Nielsen G, Stone J, Lee TC, et al. Specialist physiotherapy for func-
TABLE S1. Clinical trials investigating therapeutic interventions
tional motor disorder in England and Scotland (Physio4FMD): for Functional Movement Disorder.

MOVEMENT DISORDERS CLINICAL PRACTICE 2025. doi: 10.1002/mdc3.70136 15