Functional Movement Disorder: Evolving Mechanisms, Diagnostic Precision, and Personalized Multidisciplinary Care

Abstract

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 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 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. 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 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 disabling condition seen across neurological practice. Historically labeled as hysteria, psychogenic, dissociative, or conversion disorder, ¹ FMD is now understood as a neuropsychiatric condition arising from the complex interaction of neurobiological, psychological, and social factors. This redefined framework reflects advances in neuroimaging and neurophysiology that demonstrate abnormalities in brain networks involved in motor control, attention, emotion regulation, and self‐agency without evidence of structural lesions. ²

The diagnostic process has transitioned from an exclusion‐based approach to one based on identifying positive clinical signs. Misdiagnosis can lead to ineffective treatments and prolonged disability. Coexistence with structural neurological disorders adds to the diagnostic challenge. ³

This narrative review summarizes current knowledge on the epidemiology, pathophysiology, clinical features, and treatment of FMD. It incorporates neuroimaging and electrophysiological findings to describe the altered sensorimotor and affective networks associated with symptoms. FMD is presented as a treatable neurological disorder, emphasizing the need for multidisciplinary and individualized management approaches that integrate scientific evidence with empathetic clinical care.

Methods

A narrative approach was chosen due to the broad scope of the topic and the heterogeneity of available data. A structured search of PubMed identified peer‐reviewed articles published between January 2015 and March 2025 using terms related to FMD and its subtypes. Eligible studies included original clinical research, interventional trials, and broader functional neurological disorder (FND) studies with relevant data on motor manifestations. Review articles, single case reports, and studies lacking methodological transparency were excluded.

The search yielded 1758 articles. Following exclusions, 324 studies remained, including 15 case series, 284 observational studies, and 24 clinical trials. The final selection of articles was based on the authors’ consensus. Further details are available in the Supplementary Material.

Results

Epidemiology

FMD is more prevalent than historically recognized. ⁴ Fahn reported FMD in 0.6% of 2500 movement disorder patients, rising to 1.6% when including suspected functional origins. Among 1200 dystonia patients, 1.8% had a functional diagnosis. ⁵ Ertan and colleagues found a prevalence of 2.8% in 1743 patients. ⁶ Stone et al reported that 15.5% of 3781 new neurology referrals met FND criteria, including 1.5% with FMD. ⁷ Other studies estimate FMD affects 3–10% of new movement disorder clinic patients, ⁸ , ⁹ and 5–10% of referrals without Parkinson's disease. ¹⁰ , ¹¹ A recent cohort study reported that 18.3% (80 of 437) of neurology patients had FND, including eight with FMD. ¹² FMD occurs more frequently in women (2:1 to 5:1). ⁵ , ⁶ , ¹³ A meta‐analysis including 4905 cases found 72.6% were female, with mean onset at 39.6 years. Women present slightly earlier than men (39.1 vs 41.0 years). The age distribution shows two peaks: late adolescence (16–22 years) and midlife (35–45 years). Common clinical presentations include mixed FMD (23.1%), tremor (21.6%), and weakness (18.1%). Functional dystonia presents earlier (34.5 years), whereas gait disorder manifest later (43.2 years). While parkinsonism and myoclonus are more frequent in men, most subtypes predominate in women. ¹⁴

Earlier reports suggested no racial or ethnic predisposition, but recent data highlight the need for a more detailed demographic analysis. ⁹ , ¹⁴ , ¹⁵ , ¹⁶

In pediatric populations, FMD mirrors adult presentations but may follow a more benign course with a better prognosis. Reported prevalence ranges from 2.8% to 23.1%, with higher rates in girls. ¹⁷ Tremor and dystonia remain the predominant subtypes. ¹⁸ , ¹⁹

FMD occurs less often in older adults. In a study of 117 patients aged 62–70, only 18 developed symptoms after age 60. Tremor (61.1%) and dystonia (38.8%) were the most common, with identifiable stressors (mostly family‐related) in 83.3% and psychiatric comorbidities in 33.3%. ²⁰

FMD frequently coexists with non‐functional neurological disorders (10–15% of cases). ²¹ , ²² Known risk factors include sexual abuse, post‐traumatic stress disorder, alcohol misuse, suicide attempts, and significant psychosocial stressors such as divorce or bereavement. ¹³ , ²³ , ²⁴ , ²⁵ Social dynamics also modulate FMD incidence; the COVID‐19 pandemic corresponded with increased FMD presentations in both pediatric and adult populations in the USA. ²⁶

Classification

No standardized classification system currently exists for FMD. Despite shared clinical features—variability, distractibility, and inconsistency—it manifests across multiple phenotypes, including tremor, weakness, dystonia, gait abnormalities, jerks, tics, and myoclonus.

Subclassifying FMD into discrete phenotypes remains clinically valuable, as subtypes differ in age of onset, sex distribution, and treatment response. ¹⁴ This “splitting” approach may reveal phenotype‐specific mechanisms and guide therapy. Support for this framework comes from studies identifying distinct FMD clusters. One analysis described two predominant subgroups: the first included older patients with functional tremor and parkinsonism, often accompanied by anxiety and more responsive to pharmacological treatments. The second group comprised younger individuals with functional weakness, frequently reporting comorbid symptoms like headache, pain, and visual disturbances, and better managed with antidepressants. ²⁷

However, the clinical relevance of this “splitting” model remains debated. Tinazzi and colleagues reported substantial demographic and clinical characteristics overlap across FMD subtypes, suggesting a shared pathophysiological basis. ²⁸ Furthermore, longitudinal data show that nearly half of the patients experience shifts in their dominant movement disorder phenotype over time, challenging the stability and utility of rigid subtype classification. ²⁹

Recent studies propose alternative frameworks that account for both motor and non‐motor dimensions. Gilmour et al introduced a classification that distinguishes between episodic and constant symptom profiles. ³⁰ Patients with episodic FMD often exhibit hyperkinetic movements, anxiety, hyperarousal, and trauma‐related symptoms—features that may require trauma‐focused and emotion‐regulation–based therapies. In contrast, patients with constant FMD more commonly present with fixed dystonia, gait disturbance, and weakness, along with a reduced sense of agency and behavioral avoidance, supporting the use of motor retraining and psychologically informed rehabilitation.

Emerging classification systems may benefit from integrating clinical features—symptom profile, age at onset, psychiatric comorbidities, functional impairment—with biomarkers, including amygdala reactivity and altered functional connectivity. ³¹ A multidimensional approach may improve diagnosis, clarify mechanisms, and guide personalized treatment.

Pathophysiology and Etiopathogenesis

FMD and other FND result from complex neurobiological, psychological, and social interactions. The biopsychosocial model frames FMD as a disorder influenced by predisposing, precipitating, and perpetuating factors rather than a purely neurological or psychiatric condition (Fig. 1). ³²

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.

Predisposing factors include abnormal sensorimotor integration, prior neurological illness, and genetic susceptibility. Psychological traits—particularly anxiety, depression, emotional dysregulation, and dissociative tendencies—contribute to symptom development. Early‐life trauma or adverse experiences increase the risk, while acute stressors—injury, panic attacks, or life events—often trigger onset. Maladaptive brain responses to pain, dysfunction, or uncertainty, along with social stressors such as financial instability, relational conflict, and lack of support, can contribute to symptom persistence. Clinical reinforcement, including extensive diagnostic testing to exclude structural disease, disability benefits, or the belief that symptoms are irreversible, may contribute to symptom worsening and chronicity. ³³ , ³⁴

Research on FND has identified abnormalities in sensory processing, motor output, cognitive control, or combinations thereof, with FMD mainly affecting motor circuits. ⁸ , ¹¹ , ²¹ , ³⁵ Cognitive neuroscience highlights four core dysfunctions: altered attentional control, emotional dysregulation, impaired sensorimotor integration, and disrupted bodily self‐awareness. ³⁶ These dysfunctions implicate salience, agency, emotion regulation, and interoception networks. Whether these disruptions are predisposing factors or consequences of chronic symptoms is unclear, though a bidirectional model, where psychosocial stress alters brain function and reinforces maladaptive motor patterns, is plausible. ³⁴ , ³⁷

Predictive coding models propose that FMD results from disrupted integration of sensory input and motor predictions, leading to a reduced sense of agency. ³⁶ Affective and attentional biases shape prior expectations, which override top‐down predictions and distort sensory processing. Electrophysiological and behavioral data support this, showing cognitive biases favoring expectations over sensory evidence. ³⁸ Slowed sensory processing and reduced attention to interoceptive cues may enhance feedforward errors. For example, individuals with functional dystonia show higher pain tolerance despite normal thresholds, indicating a dissociation between sensory and emotional pain components. ³⁹ Heightened emotional salience may impair voluntary motor control, favoring automatic actions. ⁴⁰ Executive dysfunction, possibly from excessive attentional demands, may contribute to fatigue and concentration issues. ⁴¹ Biomarkers have been reported, such as absent contingent negative variation and reduced decision‐making drift rate. ³⁸ , ⁴² Patients also show attentional bias away from emotional faces and impaired impulse inhibition. ⁴³ , ⁴⁴ In functional gait disorder, maladaptive motor patterns and prolonged de‐adaptation may stem from motor planning deficits and anxiety. ⁴⁵

Functional neuroimaging shows altered connectivity in multiple brain networks. Dorsal attention network disruption may impair goal‐directed motor control. Sensorimotor and temporoparietal junction dysfunctions correlate with impaired feedforward signaling and reduced agency. Salience and limbic network abnormalities are associated with interoceptive and emotional dysregulation. Ventral attention network deficits may compromise stimulus‐driven attention. ³⁶

FND patients show increased limbic reactivity to emotional stimuli, including heightened amygdala activation, elevated cortisol levels, and altered heart rate variability. ³⁴ , ⁴⁶ Failure to habituate to negative stimuli may contribute to persistent stress responses. ⁴⁷ Dysregulated midbrain and prefrontal regions activation during emotional tasks suggest impaired behavioral–motor responses to perceived threats. The amygdala, influenced by early‐life trauma and cortisol exposure, plays a central role in FMD pathophysiology. Structural and functional changes—including increased dendritic complexity and synaptic density—lead to excitatory‐inhibitory imbalance and hyperactivity, disrupting motor and executive control network regulation. ³² , ³⁶ , ⁴⁷ , ⁴⁸ , ⁴⁹ , ⁵⁰ , ⁵¹ , ⁵² , ⁵³ , ⁵⁴ Neuroimaging reveals hypoactivation of the contralateral primary motor cortex and parietal regions, with concurrent hyperactivation in the amygdala, temporoparietal junction, and insula. ³¹ During emotion regulation tasks, FMD patients show increased activity in self‐referential and interoceptive regions, suggesting altered self‐processing. ⁵⁵ Increased anterior cingulate cortex activation correlates with emotional dysregulation and may predict treatment response. ⁵⁶ , ⁵⁷ The enhanced amygdala‐motor area connectivity suggests limbic‐motor coupling as a key mechanism underlying involuntary motor symptoms.

Structural imaging studies report gray matter and subcortical volume differences—particularly in the basal ganglia, thalamus, and insula—associated with symptom severity, dissociation, and childhood trauma. ⁵⁸ Machine learning models can distinguish FND patients from controls based on neuroimaging data. ⁵⁹ In FMD, microstructural changes in limbic and associative tracts suggest altered internal and external cues integration. ⁶⁰ Structural differences in the temporoparietal junction and putamen may relate to impaired self‐agency and prediction error. ⁵⁹

Clinical Characteristics of Functional Movement Disorder

FMD presents with a broad spectrum of involuntary motor symptoms—including tremor, weakness, dystonia, gait abnormalities, myoclonus, and tics—that are characteristically inconsistent, variable, and often incongruent with known structural neurological diseases. ³⁵ Many patients demonstrate preserved motor function under specific conditions, such as distraction or dual‐task testing, while emotional stimuli frequently exacerbate symptoms. ⁴⁷

Despite ongoing debate on whether FMD should be conceptualized as a unitary disorder or a group of phenotypically distinct subtypes, subclassification remains clinically useful for diagnosis and treatment. ²⁸ This review adopts a subtype‐oriented perspective and describes the clinical features of the most common phenotypes for educational and practical purposes.

Despite this classification, mixed motor phenomenology remains the most frequent presentation. In a study by Gilmour and colleagues, more than half (53%) of patients exhibited more than one motor symptom. ³⁰

Non‐motor symptoms are also highly prevalent and contribute significantly to disability. Pain (84%) and fatigue (65%) are common across all motor phenotypes. ³⁰ Psychiatric comorbidities, especially anxiety, depression, and trauma‐related symptoms, are also frequent.

Tinazzi et al reported that 45.8% of patients had combined movement phenotypes, and 83.9% experienced at least one non‐motor symptom, most commonly anxiety (52.1%), fatigue (45.1%), and pain (41.9%). ⁶¹ In a separate study, pain was more frequent in functional dystonia (47.4%) than in functional tremor (17.5%). Functional weakness was associated with a higher prevalence of sensory disturbances (51.7%) compared to tremor (7.5%), dystonia (5.3%), or gait disorder (11.8%). ²⁸

Other non‐motor features—including insomnia, dissociative symptoms, and depersonalization—also contribute to the clinical profile, although their prevalence does not appear to differ substantially across motor subtypes. These findings underscore the importance of a holistic diagnostic framework that considers both motor and non‐motor dimensions of FMD and the high degree of clinical overlap across subtypes.

Functional Tremor

Functional tremor, the most common FMD subtype, represents 40–50% of cases in specialist clinics. ⁵ , ⁶ , ⁸ , ¹¹ , ¹⁸ , ²¹ , ⁶² A meta‐analysis found it in 21.6% of FMD patients, with a female predominance of 72.9%. ¹⁴ Unlike non‐functional tremors, it presents with rhythmic, involuntary jerks, typically of sudden onset and non‐progressive course. Clinical features include spontaneous remissions, paroxysmal exacerbations, the coexistence of rest, postural and action tremors, and fluctuating frequency and amplitude. ⁶³ , ⁶⁴ , ⁶⁵ , ⁶⁶ , ⁶⁷ , ⁶⁸ , ⁶⁹ , ⁷⁰ Symptoms are often modulated by cognitive or emotional factors, serving as diagnostic clues.

Tremor usually affects the limbs bilaterally and symmetrically, with frequencies ranging from 4 to 10 Hz, and may involve the head or voice. Coexisting functional movement symptoms, including dystonia and myoclonus, are common, while associations with functional parkinsonism, tics, or dyskinesias are less frequent. ⁶⁸ , ⁶⁹ , ⁷⁰

Functional tremor often intensifies with focused attention and improves with distraction, although this can also occur in parkinsonian tremor. A key feature is the coactivation sign, where agonist and antagonist muscles activate simultaneously, leading to irregular, jerky, or inconsistent movements. ⁶⁵ Another hallmark is entrainment, where tremor frequency synchronizes with voluntary rhythmic tasks, such as finger tapping. Functional tremor may spread to adjacent body parts or generalize but rarely affect the fingers. ⁶⁴ Exaggerated slowness and inconsistency across tasks, sometimes called the “whack‐a‐mole sign,” can also aid diagnosis.

Electrophysiological assessments, such as electromyography and accelerometry, often show marked amplitude, direction, and frequency variability. ⁷¹ Approximately half of the patients have tremor rhythm coherence across muscle groups. ⁷²

Functional Dystonia

Functional dystonia is the second most common phenotype of FMD, though some reports place it third after myoclonus. Its diagnosis is challenging due to the lack of definitive biomarkers to distinguish it from idiopathic dystonia, often leading to misclassification. Initial reports on functional dystonia emerged in 1975, with case presentations at the 1983 American Academy of Neurology meeting. ⁷³

Estimates suggest functional dystonia accounts for 2.2% to 12% of dystonia cases and 11.8% of FMD patients. ¹⁴ , ⁷⁴ , ⁷⁵ , ⁷⁶ Two seminal case series by Fahn and Williams and Lang provided insights into its clinical presentation. Fahn and Williams described 39 patients (mean age 26 years, SD 13.6; two male), including seven with paroxysmal and 14 with continuous dystonia. Common features included inconsistent dystonic postures (18 patients), functional weakness (14), sensory disturbances (5), somatization symptoms (8), functional seizures (5), and co‐occurring FMD (7). Nine achieved complete remission, and four showed significant improvement. ⁷⁴ Lang's series (18 patients, mean age 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 symptoms, and 15 had functional neurological comorbidities. ⁷⁷

Functional dystonia typically presents with fixed, abnormal postures, sometimes following minor trauma. Diagnosis relies on positive clinical features such as inconsistency and variability (Table 1). ⁷⁸ , ⁷⁹ , ⁸⁰

TABLE 1.

Clinical features supporting a diagnosis of Functional Movement Disorder

Patient history	Physical examination
• Sudden or abrupt symptom onset • Clear triggers such as physical injury, illness, or psychological stressors • Spontaneous remissions or marked symptom fluctuations • History of childhood trauma or adverse life events • Psychiatric comorbidities (eg, anxiety, depression, PTSD) • Family history of functional neurological or psychiatric disorders • Detailed, emotionally charged descriptions of symptom onset	Inconsistency • Variability: Movement characteristics (eg, tremor amplitude or frequency) change across time or context • Distractibility: Symptoms diminish or resolve when attention is diverted (eg, mental arithmetic) • Suggestibility: Symptom intensity alters in response to verbal suggestion or clinician focus • 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

Recent studies continue to investigate the neurophysiological basis of functional dystonia. In functional torticollis, EMG recordings show abnormal autospectral peaks in the sternocleidomastoid and splenius muscles, which are not seen in non‐functional cases. ⁸¹ Espay et al reported that patients with functional dystonia have altered cortical and spinal excitability similar to structural dystonia, suggesting possible shared mechanisms. ⁸²

Functional Myoclonus

Functional myoclonus is characterized by involuntary, irregular jerks with variable amplitude, frequency, and distribution, unlike the consistent patterns in structural myoclonus. Monday and Jankovic's study of 18 patients (mean age 49.5 years) found segmental myoclonus in 10, generalized in 7, and focal in 1. Onset was abrupt in most (n = 11), with symptoms worsening under stress (n = 15). Distraction improved symptoms in 14 patients and placebo in 9, suggesting modifiability as a diagnostic clue. ⁸³ Functional axial jerks represent a common manifestation. ⁸⁴

Electrophysiological studies aid in distinguishing functional from structural myoclonus. EMG shows prolonged muscle bursts (>100 ms), no triphasic activation between agonist and antagonist muscles, and delayed latencies, contrasting with the short, synchronized bursts of cortical or subcortical myoclonus. ⁸⁵

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 and a late component related to execution. ⁸⁶ In patients with functional myoclonus, a BP preceding jerks suggests voluntary motor preparation, supporting functional etiology. ⁸⁷ However, the clinical utility of BP is limited by its relatively low sensitivity. In one study, BP was detectable in only 63% of cases, ⁸⁸ demonstrating high specificity but restricting its standalone diagnostic value. ⁸⁹ Consequently, the diagnosis of functional myoclonus remains primarily clinical, guided by the presence of positive signs such as variability, distractibility, and entrainment, and supported by electrophysiological findings when available.

Functional Parkinsonism

Functional parkinsonism, a rare and challenging phenotype of FMD, was first described in 1988. ⁹⁰ It remains under‐recognized due to its clinical overlap with neurodegenerative parkinsonian syndromes and variable presentation. Lang et al reported 14 cases (7 male), most showing features of functional parkinsonism, including rest tremor with inconsistent frequency (12 patients), rigidity reflecting voluntary resistance (6), and incongruent bradykinesia, gait disturbances, or postural instability (12). ⁹¹

Key clinical signs include slowness during repetitive movements, lacking the decremental pattern of idiopathic Parkinson's disease, variable resistance to passive movement without cogwheel rigidity, and exaggerated effort (the “huffing and puffing” sign). These features and fixed postures suggest a functional origin rather than structural parkinsonism. ⁹²

Functional parkinsonism can co‐occur with idiopathic Parkinson's disease, complicating diagnosis as functional symptoms may mask structural pathology. ⁹³ , ⁹⁴ , ⁹⁵ Accurate diagnosis relies on a thorough clinical assessment supported by electrophysiological studies and, when needed, SPECT imaging. With careful longitudinal observation, diagnosis remains primarily clinical, focusing on signs of inconsistency, variability, and distractibility.

Functional Gait Disorder

Functional gait disorder (FGD) involves abnormal walking patterns without a consistent neurological basis and remains diagnostically challenging due to their variability. Although no standardized classification exists, early descriptions by Roussy and Lhermitte included patterns such as astasia‐abasia, pseudotabetic gait, and pseudopolyneuritic gait. Other reported types include narrow‐base “tightrope” gait, stiff “robot‐like” gait, limping, choreiform movements, and theatrical or unusual patterns like walking on a “sticky surface” or through water. ¹¹

Rubino later categorized FGD as a higher‐level gait disorder, alongside cautious gait, frontal lobe gait disorders, gait initiation failure, and primary progressive freezing of gait. ⁹⁶ In 60 cases, Keane found ataxic gait most common (40%), followed by hemiparetic (21.7%), paraparesis‐like (16.7%), and tremulous gaits (18%). ⁹⁷ Baik and Lang, in a larger cohort (n = 279), noted that excessive slowness, including in gait, was more common in pure FMD cases. ⁹⁸

Characteristic features of FGD include variability with suggestion or distraction, excessive slowness or hesitation, exaggerated unsteadiness without falling, and signs like a functional Romberg (marked swaying without sensory or vestibular deficits), “walking‐on‐ice” gait (short, cautious steps with stiff knees and ankles), and sudden knee buckling without true collapse. ⁹⁹ , ¹⁰⁰ , ¹⁰¹

While diagnosis is primarily clinical, ancillary tools—such as stabilometry, posturography, and vertical plane kinematic analysis—can help distinguish FGD from subtle cerebellar, sensory, or pyramidal disorders. ¹⁰² , ¹⁰³ , ¹⁰⁴

FGD often coexists with other FMD and non‐motor symptoms like fatigue, pain, or dissociation. Recognition of inconsistency and incongruence through focused neurological examination is key for diagnosis.

Functional Tics

Functional tics have gained attention due to a notable rise in cases following the COVID‐19 pandemic, particularly among adolescents and young adults. ¹⁰⁵ , ¹⁰⁶ , ¹⁰⁷ Defined as sudden, rapid, recurrent, non‐rhythmic motor movements or vocalizations without a structural basis, ¹⁰⁸ their pre‐pandemic prevalence was estimated at 4–5% of FMD cases, ⁶ , ¹⁰⁸ , ¹⁰⁹ though recent studies report rates from 2% to 32%, depending on criteria. ¹⁰⁹ , ¹¹⁰ Many cases present acutely, often in females, following psychosocial stressors. ¹¹¹

Functional tics share features with primary tic disorders, including sudden onset, distractibility, stereotypy, suggestibility, and fluctuating symptoms. ¹⁰⁹ , ¹¹² , ¹¹³

However, they more commonly emerge after age 12, following identifiable physical or psychological triggers. Symptoms usually begin abruptly and are severe at onset. A family history of tics is typically absent. They are more variable and inconsistent than primary tics, often lacking the rostrocaudal progression or waxing‐and‐waning pattern of Tourette's syndrome. Additional features include entrainment, blocking tics, and exaggerated palilalia, echolalia, or coprolalia‐like behaviors. ¹⁰⁸ , ¹⁰⁹ , ¹¹² , ¹¹³ , ¹¹⁴

Functional tics frequently co‐occur with other FMD, autism spectrum traits, anxiety, or depression. Pharmacological treatments for primary tic disorders are often ineffective, while behavioral therapy and stress management provide better outcomes. ¹⁰⁸

Premonitory urge—a subjective sensation preceding tic execution—was once considered a possible distinguishing feature. ¹¹⁵ However, recent evidence indicates it lacks sufficient diagnostic specificity. ¹¹⁶

Other Forms of Functional Movement Disorder

Beyond common FMD phenotypes, less frequent but clinically relevant presentations exhibit hallmark FMD features, including variability, inconsistency, and incongruence with known neurological patterns.

Functional chorea involves continuous, flowing, irregular or non‐patterned movements lacking the stereotypy and rhythmicity of neurodegenerative chorea. ¹¹⁷ Functional hemiballismus presents with abrupt, exaggerated, large‐amplitude flinging movements without the subthalamic lesion typical of structural cases. Similarly, functional hemifacial spasm causes unilateral facial twitching that does not follow classic facial nerve pathology. ⁶ , ¹¹⁸

Other forms include functional stomatognathic disorders (jaw clenching, tongue thrusting), ¹¹⁹ , ¹²⁰ functional eye movement disorders (irregular gaze shifts, ptosis, eyelid fluttering), ¹²¹ and functional palatal tremor—rhythmic, soft palate, uvula, or pharyngeal 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—also exhibit abrupt onset, distractibility, and fluctuation. ¹²³ , ¹²⁴

Functional camptocormia, marked by involuntary forward trunk flexion, improves when supine—distinguishing it from other causes such as parkinsonism or myopathy. ¹²⁵

Functional writer's cramp mimics task‐specific dystonia but lacks consistent activation patterns, ¹²⁶ while functional ataxia presents with unsteady gait, limb incoordination, or exaggerated postural sway that improves with distraction. ¹⁰⁴

Diagnosis

The diagnostic approach to FMD has evolved significantly from exclusion to a rule‐in strategy based on positive signs, improving confidence and enabling earlier intervention.

In 1988, Fahn and Williams proposed a diagnostic framework for psychogenic dystonia, later expanded to all FMD subtypes. ⁷⁴ It classified FMD into four levels of diagnostic certainty: documented FMD, supported by direct evidence (eg, response to suggestion or psychotherapy); clinically established FMD, based on incongruent signs and psychiatric comorbidities; probable FMD, with suggestive features but lacking definitive evidence; and possible FMD, with insufficient positive signs but potential psychiatric associations. ²² , ⁶³ , ¹²⁷ This classification was later revised to improve inter‐rater reliability. The inclusion of psychiatric symptoms aimed to enhance specificity but had limitations, as these features are neither exclusive to FMD nor always present. ¹²⁸ These challenges led to a broader reconsideration of diagnostic approaches.

The most significant paradigm shift emerged with the publication of the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM‐5), which established positive clinical signs—such as inconsistency and incongruence—as the cornerstone of diagnosis. The DSM‐5 reframed FMD under the umbrella of 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

The term psychogenic once included somatoform conditions, factitious disorder, and malingering, ⁸ but these are now recognized as distinct from FMD. Factitious disorder involves intentional symptom production for the sick role, while malingering serves external incentives (eg, financial or legal gain), whereas FMD presents with involuntary symptoms. ¹³⁰ , ¹³¹ Symptom exaggeration may occur but is not inherent to FMD and is seen in other chronic conditions. Clear differentiation is essential to reduce stigma and ensure appropriate care.

Accurate FMD diagnosis requires a patient‐centered neuropsychiatric evaluation. ¹³² Positive signs—variability, distractibility, entrainment, and incongruence—help distinguish FMD from mimics, improving accuracy and reducing unnecessary testing and hospital visits. ¹³³ A structured five‐phase diagnostic process has been proposed to guide assessment, enhance communication, and support early intervention through multidisciplinary collaboration. ¹³⁴ , ¹³⁵ This approach ensures timely diagnosis, patient validation, and appropriate rehabilitation (Fig. 2).

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.

Phased Diagnostic Process for Functional Movement Disorder

Phase 1: Clinical History and Symptom Assessment

A detailed clinical history is essential for diagnosing FMD. Clinicians should assess motor and non‐motor symptoms, psychiatric comorbidities, and systemic complaints, prioritizing the most disabling symptoms. Key aspects include age and mode of onset (sudden vs gradual), potential triggers (eg, trauma, illness, surgery), and the pattern of symptom evolution, including fluctuations, variability across settings, and functional impact. Exacerbating (eg, stress, fatigue, pain) and relieving (eg, distraction, relaxation) factors offer diagnostic clues. ¹³⁶ It is also important to explore the patient's beliefs about symptom origin, perceived impact, recovery expectations, and past diagnostic experiences, including misdiagnosis, medical trauma, or invalidation, which may influence illness behavior and treatment engagement.

Phase 2: Neurological Examination for Positive Signs

A focused neurological examination is essential to identify positive signs inconsistent with structural neurological disease. Table 1 summarizes key features. In tremor, entrainment—tremor frequency modulation during contralateral movement—and the whack‐a‐mole sign, where tremor shifts to other body parts under resistance, support diagnosis. For weakness, Hoover's sign shows preserved strength during contralateral hip flexion despite apparent ipsilateral hip extension weakness, and give‐way weakness involves abrupt loss of resistance. Gait tests, such as the windmill sign (flailing arms during retropulsion) and the chair test (ability to move a chair despite gait complaints), reveal inconsistency. These findings support a rule‐in diagnosis of FMD.

Phase 3: Diagnostic Confirmation and Exclusion of Other Conditions

FMD is diagnosed clinically using positive signs, but further testing may be needed to exclude coexisting neurological disease. Investigations should be guided by phenotype. Symptoms suggesting motor neuron disease, cerebellar dysfunction, or parkinsonism may require neuroimaging or laboratory tests. ¹³⁷ Neurophysiological assessments such as surface electromyography or tremor analysis can aid diagnosis in selected cases. Lack of response to treatments like propranolol for tremor is not diagnostic, as it can occur in both functional and non‐functional disorders. Psychiatric comorbidities—including depression, anxiety, and post‐traumatic stress disorder—should be assessed, as they influence prognosis and treatment, though they are not required for diagnosis.

Phase 4: Diagnostic Communication and Patient Education

Effective, empathetic communication is central to patient understanding and acceptance of the diagnosis. Clinicians should emphasize that the diagnosis is based on objective signs, reinforcing that symptoms are genuine, involuntary, and treatable. Simple metaphors, such as comparing FMD to a “software problem,” can aid understanding. Demonstrating positive signs during the exam builds trust and reduces uncertainty. Validated educational resources, including websites, support groups, and handouts, can facilitate patient engagement and support.

Phase 5: Follow‐Up and Long‐Term Monitoring

Sustained follow‐up is essential to reinforce the diagnosis, monitor progress, and adjust treatment. Management should begin soon after diagnosis and involve a multidisciplinary team comprising neurologists, physiotherapists, psychologists, and other specialists trained in functional disorders. Regular visits help identify barriers to recovery and prevent relapse. Reviewing positive signs and maintaining open, supportive communication is important if doubts arise. An open‐door policy for re‐evaluation fosters trust and accommodates changing patient perspectives.

Treatment

Treatment of FMD has evolved significantly over the past decade, with increasing evidence supporting a multidisciplinary approach that combines physical rehabilitation, psychological therapies, neuromodulation, pharmacological interventions, and digital tools. Analysis of 24 clinical trials conducted since 2015 demonstrates promising outcomes across a range of modalities. To aid clinical decision‐making, we have synthesized these results into a structured overview of therapeutic efficacy and feasibility (Supplementary Table S1).

Cognitive behavioral therapy (CBT) is a consistently effective intervention for FMD. Espay et al ⁵⁶ reported symptom and neural activity improvements in functional tremor, while Richardson et al ¹³⁸ found CBT reduced cognitive biases. When combined with physiotherapy, it enhances the quality of life. ¹³⁹ A telehealth CBT pilot showed high adherence but no primary outcome changes. ¹⁴⁰ In children with functional tic‐like behaviors, psychoeducation groups were beneficial. ¹⁴¹ CBT alone or with physical activity reduced symptoms, ¹⁴² and nocebo hypothesis CBT sometimes led to rapid recovery. ¹⁴³

Physiotherapy, both in‐person and via telemedicine, also plays a central role in treatment. Nielsen et al ¹⁴⁴ reported objective motor improvement following physiotherapy, and Demartini et al ¹⁴⁵ confirmed the feasibility of delivering this treatment remotely. However, results from the large Physio4FMD trial revealed no significant difference between specialist physiotherapy and standard care, despite subjective reports of benefit, underscoring the importance of individualized treatment planning. ¹⁴⁶

Neuromodulation techniques have shown variable but encouraging outcomes, such as repetitive transcranial magnetic stimulation (rTMS) and intermittent theta burst stimulation (iTBS). Taib et al ¹⁴⁷ demonstrated that rTMS improved motor function in functional tremor, while Park et al ¹⁴⁸ reported limited efficacy with transcranial direct current stimulation (tDCS) combined with yoga. McWhirter et al ¹⁴⁹ and Garcin et al ¹⁵⁰ found cortical modulation effects with TMS, though clinical benefits were less pronounced. More recently, Spagnolo et al ¹⁵¹ showed that iTBS targeting corticolimbic networks improved symptom control and enhanced functional connectivity.

Pharmacological treatments have limited evidence. Botulinum toxin (BoNT) was no better than placebo in jerky/tremulous FMD, though placebo effects were notable. ¹⁵² Similarly, BoNT prior to CBT did not enhance outcomes in functional dystonia. ¹⁵³

Digital and technology‐assisted therapies are emerging. Virtual reality (VR)‐based interventions, such as mirror visual feedback and exposure therapy, have shown potential. ¹⁵⁴ Smartphone‐based tools offer accessible, low‐cost interventions that reinforce self‐management strategies. ¹⁵⁵

Evidence supports multidisciplinary treatment, combining physical rehabilitation and psychological support. Early trials of neuromodulation and digital therapies are promising, but further research is needed to confirm long‐term efficacy and identify suitable candidates. A structured therapeutic algorithm is outlined in Table 2. ¹⁵⁶

TABLE 2.

Therapeutic algorithm for Functional Movement Disorder

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

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

Prognosis

FMD prognosis varies widely and is influenced by multiple factors, 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 disabling symptoms, ¹⁵⁷ and another study reported symptom persistence in up to 90% after 3.2 years. ²³

Treatment‐based studies offer more favorable outcomes. Factor et al ⁸ reported symptom resolution in 35% of patients at 2 years, while Williams et al ⁶² found a 25% resolution rate. In a larger cohort (n = 346), Thomas and Jankovic observed improvement in 42.4% over 8 years, while 21.2% worsened and 15.2% remained unchanged. ¹¹

Data from the Physio4FMD trial provide insights into predictors of recovery. A secondary analysis by Nielsen et al ¹⁵⁸ showed that older age and strong beliefs in symptom permanence predicted poorer outcomes, while a greater sense of control was linked to improvement. Symptom duration, fatigue, pain, and psychiatric comorbidities did not significantly influence treatment response.

Table 3 summarizes clinical predictors of recovery, which can aid in diagnostic feedback, managing expectations, and treatment planning. ² , ⁶⁷ , ¹⁵⁸ , ¹⁵⁹

TABLE 3.

Prognostic factors associated with recovery in Functional Movement Disorder

Predictors of good prognosis

Predictors of poor prognosis

• Patient‐perceived control over recovery 158 • Early and accurate diagnosis 2 • Younger age at symptom onset 2 • Shorter symptom duration 2 , 159 • Presence of tremor phenotype 2 • Belief that treatment is effective 67 , 159 • Anxiety (in some studies) a , b ,  67 , 159 • Reduction or removal of psychosocial stressors 67 , 159 • High adherence to treatment 67 • Use of specific pharmacological agents 159 • Good physical health status 159 • Positive perception of social support 159

• Older age at diagnosis 158 • Strong belief in the permanence of symptoms 158 • Delayed or missed diagnosis 2 • Psychiatric comorbidities (eg, anxiety*†, depression*, personality disorders) 2 , 67 • Traumatic or psychological precipitating events 2 , 67 • Older age at symptom onset 2 • High Beck Hopelessness Scale score 2 • Longer symptom duration* 2 , 67 , 159 • Prominent non‐motor symptoms (pain, fatigue*, cognitive dysfunction) 2 • Poor therapeutic alliance or dissatisfaction with healthcare provider 67 , 159 • Negative perception of social support 67 • 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 presentations 159 • Active smoking 67 , 159 • High suggestibility 159

^a Reported as not significantly associated with outcome in some studies.

^b Findings are inconsistent across studies.

Despite increased interest in outcomes research, the field lacks standardized, validated tools that reflect the complex and fluctuating nature of FND. ¹⁶⁰ Current measures often miss patient‐centred outcomes, and discrepancies between clinician and patient reports are common, which may hold clinical significance. These limitations hinder cross‐study comparisons and may obscure treatment effects. Outcome measures that are valid, clinically relevant, and reflect patient priorities are essential for assessing treatment efficacy and improving long‐term outcomes.

Conclusion

FMD is a complex disorder involving neurological, psychological, and social factors. Despite advances in neuroimaging and neurophysiology, diagnosis remains clinical, based on positive signs. ² The condition's heterogeneity calls for personalized treatment that considers symptom profile, cognitive style, comorbidities, and functional goals. Multidisciplinary approaches integrating neurological, psychological, and rehabilitative care offer the best outcomes.

CBT is a key treatment supported by strong evidence for improving symptoms. ⁵⁶ , ¹³⁸ Its success relies on addressing maladaptive beliefs through tailored approaches. Physiotherapy is also effective, especially when combined with psychological care. Remote delivery is feasible but requires appropriate patient selection and engagement. ¹⁴⁶ , ¹⁶¹

Neuromodulation techniques (rTMS, iTBS, tDCS) have shown inconsistent results, although individualizing stimulation parameters and targeting relevant brain networks may enhance efficacy.

Digital therapies—including VR‐based, ¹⁵⁴ apps, ¹⁵⁵ and telehealth ¹⁴⁰ , ¹⁴⁵ —expand access and offer innovative, scalable solutions, but must be adapted to patient's cognitive and emotional needs while maintaining therapeutic connection.

Patient empowerment is essential. Perceived control over symptoms strongly predicts outcomes, ¹⁵⁸ highlighting the value of education, shared decision‐making, and collaborative goals. Success depends on both treatment choice and its delivery. Clear, empathetic communication improves outcomes, while poor explanation and dismissive language worsen them. ³⁵ , ¹⁶² , ¹⁶³ , ¹⁶⁴ Framing symptoms as involuntary and treatable within a biopsychosocial model promotes engagement and facilitates recovery.

Despite progress, no validated biomarkers exist for diagnosis or treatment monitoring. Although neuroimaging and electrophysiology have revealed network‐level changes, none are suitable for clinical use. ⁵⁹ Biomarker development could improve diagnosis, prognosis, and personalized care.

The limitations of this review must be acknowledged. Despite using a structured search strategy, the final study selection was guided by the authors’ discretion, introducing potential bias. We did not conduct formal quality assessments or statistical pooling, limiting our ability to assess consistency or quantify effect sizes. Inherent to narrative reviews, these constraints should be considered when interpreting our conclusions.

In summary, improving outcomes in FMD requires an integrated, patient‐centred approach that combines scientific precision with compassionate care. Priorities for future research include biomarker development, validated outcome measures, and adaptive, individualized treatments through multidisciplinary collaboration.

Author Roles

(1) Research project: A. Conception, B. Organization, C. Execution; (2) Statistical Analysis: A. Design, B. Execution, C. Review and Critique; (3) Manuscript Preparation: A. Writing of the first draft, B. Review and Critique.

E.O.‐R.: 1B, 1C, 3A, 3B.

A.S.: 1C, 3B.

J.R.‐B.: 1C, 3B.

O.A.‐C.: 1A, 1B, 1C, 3A, 3B.

Disclosures

Ethical Compliance Statement: The authors confirm that the approval of an institutional review board was not required for this work. The authors confirm that patient consent was not required for this work. We confirm that we have read the Journal's position on issues involved in ethical publication and affirm that this work is consistent with those guidelines.

Funding Sources and Conflict of Interest: No specific funding was received for this work. The authors declare no conflicts of interest relevant to this work.

Financial Disclosures for the previous 12 months: The authors declare no additional disclosures to report.

Supporting information

TABLE S1. Clinical trials investigating therapeutic interventions for Functional Movement Disorder.

Data Availability Statement

Data sharing is not applicable to this article as no new data were created or analyzed in this study.