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Functional movement disorders

Functional movement disorders
Author:
Sarah C Lidstone, MD, PhD
Section Editor:
Howard I Hurtig, MD
Deputy Editor:
April F Eichler, MD, MPH
Literature review current through: Feb 2022. | This topic last updated: Feb 21, 2022.

INTRODUCTION — Functional movement disorder (FMD) is a subtype of functional neurologic symptom disorder (conversion disorder) in which the primary symptom is tremor, dystonia, gait disorder, or other abnormal movement. Patients with FMD have neurologic symptoms that are incongruent with known neurologic disease but are nevertheless genuine and cause distress and/or psychosocial impairment [1].

FMD is common in clinical settings, but the diagnosis is often delayed or missed, and prognosis for complete remission is generally poor. Over time, more emphasis has been placed on physical examination signs to guide diagnosis and use of evidence-based treatments, including physiotherapy and multidisciplinary rehabilitation.

This topic reviews the epidemiology, etiology and pathogenesis, clinical features, diagnosis, treatment, and prognosis of FMD. Functional neurologic symptom disorder more broadly, as well as other subtypes (eg, functional weakness and nonepileptic seizures), are discussed elsewhere:

(See "Conversion disorder in adults: Epidemiology, pathogenesis, and prognosis".)

(See "Conversion disorder in adults: Clinical features, assessment, and comorbidity".)

(See "Conversion disorder in adults: Treatment".)

(See "Psychogenic nonepileptic seizures: Etiology, clinical features, and diagnosis".)

(See "Psychogenic nonepileptic seizures: Management and prognosis".)

TERMINOLOGY — FMD is a subtype of functional neurologic symptom disorder (conversion disorder) (table 1). Although conversion disorder is the term used by the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) [1], functional neurologic symptom disorder has become preferred by many because it is etiologically neutral and usually acceptable to patients. Older terms, including psychogenic, hysterical, and nonorganic, have fallen out of favor. (See "Conversion disorder in adults: Terminology, diagnosis, and differential diagnosis".)

Subtypes of functional neurologic symptom disorder recognized by DSM-5 include (from most to least common):

Nonepileptic seizures

Weakness and paralysis

Abnormal movement

Speech symptoms

Globus sensation (swallowing symptoms)

Sensory symptoms

Cognitive symptoms

The International Classification of Diseases, 11th Revision (ICD-11) uses the term "dissociative neurological symptom disorder" for the DSM-5 diagnosis of functional neurologic symptom disorder [2]. Older versions used the term "dissociative disorders." (See "Conversion disorder in adults: Terminology, diagnosis, and differential diagnosis".)

EPIDEMIOLOGY — Population rates of FMD are not known, and most studies are small and drawn from clinical settings focusing on specific phenotypes. The incidence of functional neurologic symptom disorder more broadly is reviewed separately. (See "Conversion disorder in adults: Epidemiology, pathogenesis, and prognosis", section on 'Epidemiology'.)

Prevalence in clinical settings – FMD accounts for 2 to 10 percent of patients in movement disorder clinics [3-6]. The prevalence of FMD among patients who present with dystonia and fixed, contracted joints may be even higher. As an example, one prospective study of 41 such patients reported that criteria for functional dystonia were fulfilled in 15 (37 percent) [7]. (See 'Functional dystonia' below.)

Age of onset – FMD usually begins in middle adulthood but can affect children as young as six years and older adults [5,8-10]. The mean age at presentation is 40 years [11].

Sex ratio – Females are affected more often than males in both children and adults. In large cohort studies, the percentage of females ranges from 60 to 90 percent [11-14]. However, the sex preponderance may vary by phenotype; as an example, functional myoclonus and functional parkinsonism appear to have similar frequency in males and females [15].

Phenotype frequency – Functional tremor is the most frequent FMD phenotype, followed by functional dystonia [8,14-18]. Approximately one-quarter of patients have a mixed phenotype.  

ETIOLOGIC FACTORS — FMD, like other functional neurologic symptom disorders, is best conceptualized using a biopsychosocial model of predisposing, precipitating, and perpetuating factors. Factors can be biologic, psychological, or social, and the combination of factors is unique to each patient (table 2). None of the factors is individually causal; rather, their presence increases risk of developing the disorder.

Predisposing factors – Common risk factors for developing FMD include:

Female sex

Younger age

Emotional and personality disorders

Neurologic disease/symptoms

Coexistence of other health issues

Difficulties in interpersonal relationships

Psychiatric illness

Stressful life events and maltreatment are substantially more common in people with functional neurologic symptom disorder than in unaffected controls [19]. Emotional neglect has a higher risk than traditionally emphasized sexual and physical abuse, but many patients report no stressors. Some studies have found higher rates of childhood trauma in patients with FMD compared with sex-matched controls, while others have not [3,20-26]. Additional factors, such as the nature and timing of stressful events, may influence their role as risk factors in adulthood. (See "Conversion disorder in adults: Epidemiology, pathogenesis, and prognosis", section on 'Premorbid clinical factors'.)

Exposure to functional or organic movement disorders among friends and family (disease modeling) may also be a risk factor for developing FMD [10,27].

Precipitating factors – A precipitating factor occurring in close temporal proximity with symptom onset can often be identified in 50 to 80 percent of patients with FMD. In some cases, symptoms of panic attack are present during the precipitating event [25]. Examples of precipitating factors include [25,28]:

Physical injury or accident

Surgery, medical procedure, or medical illness

Emotional event

Neurologic disorder (eg, severe migraine, brachial neuritis, Bell's palsy, carpal tunnel syndrome)

Perpetuating factors – Factors that, if present, may perpetuate FMD symptoms are important to identify, particularly those that are modifiable. Common perpetuating factors include [26,29,30]:

Pain

Physical deconditioning

Ongoing psychosocial stress related to family, work, or school

Untreated anxiety

Intercurrent illness

Illness beliefs regarding an alternate diagnosis (may or may not be modifiable)

Comorbid psychiatric disorders

Disability-related financial benefits

Litigation

Life stress that was relieved by onset of the disorder and would likely recur if the patient were to recover

Cognitive-behavioral, neurobiologic, and psychodynamic hypotheses that attempt to explain how functional symptoms develop in the context of these factors are reviewed in more detail separately. (See "Conversion disorder in adults: Epidemiology, pathogenesis, and prognosis", section on 'Hypotheses'.)

PATHOGENESIS — FMD is a complex neuropsychiatric condition, and underlying mechanisms are an intense area of study [31]. Processes relevant to FMD include [32-37]:

Abnormal self-directed attention

Abnormal beliefs and expectations

Abnormal sense of agency (ie, a subjective sense of control) for self-generated movements

Motor learning and plasticity

Abnormal limbic-motor interface

These processes may lead to an FMD when abnormal predictions regarding movement are triggered by abnormal self-directed attention, leading to movement produced without a normal sense of voluntary control [32,38]. In patients with alexithymia (difficulty identifying and expressing emotion) or a tendency to somatize, emotional or autonomic symptoms that occur with a triggering event may be misinterpreted as being caused by a physical illness [35].

Subtle structural and functional differences between individuals with FMD and controls have been demonstrated using advanced imaging techniques. As an example, an observational study using magnetic resonance imaging (MRI) voxel-based morphometry analysis showed increased gray matter volume in left amygdala, left striatum, left cerebellum, left fusiform gyrus, and bilateral thalamus and decreased volume of left sensorimotor cortex among 35 patients with FMD compared with 35 unaffected controls, irrespective of clinical phenomenology [39]. However, other smaller studies have shown a different set of cerebral abnormalities, perhaps due to variations in methods of analysis. Similar work by the same group demonstrated impaired self-agency (the ability to control one's actions) using functional MRI, which showed a lack of connectivity between the temporo-parietal junction and sensorimotor cortex [37].

CLINICAL FEATURES

Shared features — FMD very often begins abruptly, regardless of phenotype (table 3) [11]. In a cohort of 50 patients with FMD, 54 percent of patients reported sudden onset within seconds to minutes, while 36 percent developed symptoms over the course of hours to one day [25]. By contrast, other movement disorders typically begin gradually and without provocation, except when the underlying cause is an acute illness such as a stroke.

Progression to maximum symptom severity and disability is often rapid, which is uncommon in other movement disorders. Illness, surgery, and physical injuries are common precipitants, including minor injuries (eg, lifting a moderate weight or following a nonconcussive motor vehicle accident). Often more than one type of movement disorder is present, which can be a helpful clue to the diagnosis.

Once FMD is established, abnormal movements can be present constantly or occur as discrete episodes with periods of normal functioning. Patients very often describe "good days and bad days," with variation in their function accordingly. Pain, fatigue, and cognitive symptoms are often present at a constant low level or may be the dominant symptom in some patients. Disability and unemployment due to functional symptoms or other health concerns are common but not universal.

Trials of medications and other therapeutic interventions for movement disorders have variable results in FMD, and symptoms may be much more or much less responsive than would be expected. Examples include complete remission of Parkinson-like symptoms with herbal remedies [40] and immediate resolution of fixed dystonia with injections of botulinum toxin, even though the neuromuscular blocking effect of botulinum toxin requires at least 72 hours before a clinical impact can be observed [41]. Lack of response to carbidopa-levodopa for suspected Parkinson disease should be interpreted cautiously, as poor responses can also be characteristic of atypical parkinsonism.

Functional tremor — Functional tremor is the most common type of FMD. Tremor is defined as a rhythmic and oscillatory movement of a body part with a relatively constant frequency. (See "Overview of tremor".)

Functional tremor typically occurs with rest, posture, and action. Any body part may be involved, but hand tremor, leg tremor, and whole-body tremor are common sites [42]. A feeling of "internal" tremor is common although not specific to FMD. In the upper limbs, the fingers are often spared, with much of the tremor occurring at the wrist [17,43].

There are numerous positive signs of functional tremor, including hallmark signs of distractibility, variability, and entrainability.

Distractibility – Distractibility refers to complete remission or temporary suspension of the tremor with a cognitive or motor task. A common distraction maneuver is to ask the patient to hold the arms outstretched, and once the tremor is established, ask the patient to count through each of their fingers in order on the contralateral hand. Other potent distraction techniques include the history portion of the assessment and standard cranial nerve examination [44]. (See 'Distractibility' below.)

Variability – Variability manifests as changes in tremor distribution, direction, frequency, and amplitude at different time points during the assessment, or over time on history. (See 'Variability' below.)

Entrainment – Entrainment refers to a shift of tremor frequency to match an externally or internally directed competing rhythmic movement with another body part. Some patients can "self-entrain" to stop their own functional tremor. Entrainment can also be demonstrated electrophysiologically in selected cases. (See 'Electrodiagnostic testing' below.)

Co-contraction – Patients with functional tremor may have isometric contraction of antagonist muscles in the tremoring body part. This ongoing co-contraction may be perceived on examination as increased muscle tone during passive movement [43].

"Whack-a-mole" sign – Movement suppression of one body part (eg, holding an individual's wrist) may be followed by immediate re-emergence of movement in another body part [45,46].

Response to weight load – Functional tremor may increase in amplitude with weight load [47,48].

Pause with ballistic movement – Tremor may temporarily arrest, followed by ballistic movement of the contralateral arm.

Electrophysiologic studies may be helpful in distinguishing functional tremor in challenging cases with inconsistent or hard-to-elicit positive signs. (See 'Electrodiagnostic testing' below.)

Functional dystonia — Functional dystonia is the second most common type of FMD. Dystonia refers to sustained or intermittent muscle contractions causing abnormal, often repetitive movements, postures, or both. Dystonic movements are typically patterned and twisting, and may be accompanied by tremor, which is usually slow and irregular. Dystonia is often initiated or worsened by voluntary action and associated with unintentional muscle contraction (overflow muscle activation). (See "Etiology, clinical features, and diagnostic evaluation of dystonia", section on 'Clinical features'.)

Functional dystonia is often described by the patient as "spasms" and may affect any part of the body (focal) or multiple areas at once (generalized). Clinical features and positive signs fall into three main phenotypes:

Fixed focal postures – Common focal presentations of functional dystonia include fixed plantarflexion/inversion of the ankles and fixed finger flexion sparing the pincer grasp. Fixed postures are rare in nonfunctional dystonia. Patients typically display marked resistance to passive movement when the limb is at rest. Pain and sensory disturbances are often present, although not always. In severe cases, muscle atrophy or joint contractures may be present due to disuse or prolonged maintenance of the tonic posture.

Of note, most cases of dystonia after peripheral trauma are probably examples of functional focal dystonia [7,49]. The entity may be termed peripherally induced dystonia, fixed dystonia, traumatic or posttraumatic dystonia, posttraumatic cervical dystonia, posttraumatic painful torticollis, causalgia-dystonia syndrome, and complex regional pain syndrome dystonia (formerly reflex sympathetic dystrophy dystonia) [7,49-55]. In most cases, the precipitating trauma is minor. The inciting injury may involve nerve root, peripheral nerve, or soft tissue. Although the mechanism is controversial [56-62], there is little evidence to support an organic basis, while the overlap with FMD features is extensive [50].

Positive signs include the presence of a fixed posture typical of functional dystonia, dramatic/immediate resolution with interventions (eg, physiotherapy, placebo, low-dose botulinum toxin injection), and lack of dynamic features such as overflow or a sensory trick. (See "Etiology, clinical features, and diagnostic evaluation of dystonia", section on 'Dynamic and temporal features'.)

Functional cranial dystonias – Functional facial spasms are a common subtype of functional dystonia. Concomitant jaw pain is common, and dental procedures are a trigger in some patients. Facial spasms may be solitary or occur in combination with episodic generalized dystonic spasms. Platysma overactivation is often present and may be misinterpreted as lower facial weakness, such as a facial droop seen in stroke. Functional facial dystonia is remarkably consistent between individuals with recognizable features [63].

A case series of 61 patients with facial FMD showed episodic or sustained muscular spasms resembling dystonia in all patients, most commonly involving the lips (61 percent), eyelids (51 percent), perinasal region (16 percent), and forehead (10 percent) [63]. The most common pattern consisted of tonic, sustained, lateral, and/or downward protrusion of one side of the lower lip with ipsilateral jaw deviation. More than half of patients had ipsi- or contralateral blepharospasm and excessive platysma contraction in isolation or combined with fixed lip dystonia. Spasms were reported as painful in 25 percent.

Positive signs of functional facial spasms include downward lip-pulling, orbicularis oculi spasm, jaw deviation, and platysma overactivation. Signs that can help distinguish functional facial movements from those of tardive dyskinesia include lack of chewing movements or self-biting, lingual movements without mouth movements, and the presence of abnormal speech. (See "Tardive dyskinesia: Etiology, risk factors, clinical features, and diagnosis", section on 'Oro-bucco-lingual and facial dyskinesia'.)

Other common patterns include constant tonic eye closure, constant bilateral eye closure with the absence of prominent muscle activity (resembling ptosis), and contraction of corrugator and procerus muscles casing a narrowed palpebral fissure without involvement of orbicularis oculi.

Paroxysmal mixed dystonia – The most common form of generalized functional dystonia is paroxysmal mixed dystonia. These are nonstereotyped episodes, which often have mixed movements that do not conform to a single phenomenology (ie, elements of dystonia, ataxia, chorea, and ballism). Associated symptoms of pain or dissociative-like symptoms are common. Episodes may share overlapping features with nonepileptic seizures [64].

Functional gait — Functional gait disorders can occur as an isolated FMD or in combination with other FMD phenotypes. Examples of mixed FMD include functional leg weakness causing a leg-dragging gait and functional fixed lower-limb dystonia causing a dystonic gait [65].

Numerous functional gait patterns have been described, including [28,66-69]:

Excessive slowness and stiffness

Knee-buckling gait

Leg-dragging gait

Dystonic gait

Astasia-abasia, an inability to stand (astasia) or walk (abasia)

"Walking on ice"

Uneconomic gait

Bizarre gait (ie, not conforming to any of the usual patterns observed with neurologic gait disorders)

Maintenance of postural control on a narrow base with flailing arms and excessive trunk sway

Knowledge of gait patterns is essential in diagnosing functional gait disorders. The mere presence of a cautious gait does not confirm a functional etiology. A cautious gait may be a legitimate psychological adaptation, based upon an appropriate response to real or perceived disequilibrium [70]. In addition to appropriate caution and fear of falling, the differential diagnosis of cautious gait includes higher-level frontal (apraxic) gait disorders. (See "Causes and evaluation of neurologic gait disorders in older adults", section on 'Frontal (apraxic) gait'.)

Bizarre gait patterns are also not always functional and may be seen in patients with dystonia syndromes. In these cases, the diagnostic clue of a functional etiology is variability, or the inconsistency of the bizarre functional gait. By contrast, dystonic gaits will be consistently "bizarre" (ie, the same gait pattern is consistently repeated and the same deficits present at the same point in the gait cycle) [71]. An exception to this consistency occurs in patients with lower-limb dystonia, who may appear to have a foot drop when walking forward but not backward (when the dystonia consistently resolves).

Positive signs for functional gait include dragging monoplegic gait, huffing and puffing, falling toward support, excessive slowness, hesitation, noneconomic posture, and knee-buckling [72-74]. Asking a patient with gait disorder to propel themselves forwards and backwards in a rolling chair while sitting can aid in the assessment of improvement in functional gait; the adoption of a normal walking-like pattern while seated may be a positive sign [75].

Functional myoclonus — Myoclonus is a brief, shock-like muscle contraction (positive myoclonus) or a sudden lapse in tone (negative myoclonus or asterixis) of the affected body part. Patients will usually describe myoclonus as consisting of "jerks," "shakes," or "spasms." Myoclonic movements have many possible etiologies and pathophysiologic features. (See "Classification and evaluation of myoclonus".)

Functional myoclonus may be underrecognized in patients presenting with sudden body jerks, particularly when they involve the trunk or axial muscles. In one systematic review of 179 published cases identified as having propriospinal myoclonus, functional myoclonus was diagnosed in 57 percent [76]. Characteristics that suggest functional myoclonus include [77]:

Inconsistent character of the movements (amplitude, frequency, and/or distribution)

Associated functional symptomatology

Marked reduction of the myoclonus with distraction

Spontaneous periods of remission

Acute onset and sudden resolution

Evidence of underlying psychopathology

Positive signs for functional myoclonus/jerks, as with tremor, include variability and distractibility. The localization can help diagnostically, as functional jerks are often axial when other types of myoclonus occur in the limbs. Arrhythmic jerks of the trunk, hips, and knees, classically recognized as propriospinal myoclonus, can also be functional when positive signs are present (distractibility, variability) [3]. (See 'Distractibility' below and 'Variability' below.)

Electrodiagnostic testing can also be helpful in differentiating functional myoclonus from other myoclonus. Patients with functional startle tend to have an exaggerated initial startle response that habituates to repetitive stimulation but shows inconsistent latencies [78]. (See 'Electrodiagnostic testing' below.)

Functional parkinsonism — The cardinal motor manifestations of parkinsonism are rest tremor, bradykinesia, rigidity, and postural instability (see "Clinical manifestations of Parkinson disease", section on 'Cardinal features'). Manifestations of functional parkinsonism can be superficially similar but have features suggesting a functional origin, including the presence of other functional signs and symptoms [79].

Tremor – The tremor of functional parkinsonism shares the characteristics of isolated functional tremor (see 'Functional tremor' above), manifesting as a complex resting, postural, and action tremor with abrupt onset, a static course, and changeable features [28,80-82]. Movements may include violent shaking of one arm or generalized violent shaking [79]. The tremor will typically increase with attention and decrease with distraction [42].

Bradykinesia – Functional bradykinetic movements are slow and effortful but lack the typical decrement in speed or amplitude that is observed with successive movements in true bradykinesia (ie, slowing without decrement).

Rigidity – A functional increase in muscle tone is the result of gegenhalten/paratonia rather than true rigidity (ie, involuntary resistance to passive movement). Cogwheeling is absent. Of note, gegenhalten can also be seen in older adults, especially those with dementia.

Postural instability – Atypical gait abnormalities and postural instability are often present in functional parkinsonism. Postural stability testing may reveal positive signs such as arm-flailing and reeling backward without falling.

In patients who have been exposed to carbidopa-levodopa as a trial, lack of a response may be suggestive of functional parkinsonism (although atypical parkinsonian syndromes are also poorly responsive to levodopa). On the other hand, many patients with functional parkinsonism have complete symptom resolution with levodopa due to a placebo effect.

Importantly, features of functional parkinsonism may coexist with Parkinson disease, and some evidence suggests that functional parkinsonism can be an early manifestation of Parkinson disease [79,83,84]. Patients with functional parkinsonism should be followed longitudinally to examine for emerging Parkinson disease. A helpful distinguishing historical feature is that functional parkinsonism will not present with a prodrome suggestive of alpha-synuclein pathology (eg, constipation, depression, anosmia, or rapid eye movement [REM] sleep behavior disorder), as seen in most patients with Parkinson disease. A notable exception is tremor-dominant Parkinson disease, which may not display these features either, at least in the early stages. (See "Clinical manifestations of Parkinson disease".)

Knowledge of atypical parkinsonian disorders is also crucial in some cases to avoid misdiagnosis. As an example, a patient presenting with a very symmetric akinetic rigid syndrome without tremor may be erroneously diagnosed with functional parkinsonism. In fact, such a presentation is common among other parkinsonian syndromes such as multiple system atrophy and progressive supranuclear palsy. (See "Multiple system atrophy: Clinical features and diagnosis" and "Progressive supranuclear palsy (PSP): Clinical features and diagnosis" and "Corticobasal degeneration".)

A normal dopamine transporter imaging study using single-photon emission computed tomography (SPECT) scan is helpful for supporting a diagnosis of either functional, drug-induced, or vascular parkinsonism, rather than nigrostriatal degeneration [85]. However, scans can change from normal to abnormal over time, and, therefore, a single test should not be used to support a diagnosis of FMD. (See 'Neuroimaging' below and "Diagnosis and differential diagnosis of Parkinson disease", section on 'DaTscan'.)

Functional tics — Tics are recurrent, semivoluntary, stereotyped movements that can be either vocal or motor, simple or complex. There is a narrow repertoire of tics in an individual, which may change over time. Tics are accompanied by a premonitory urge to perform the movement, discomfort if the tic is contained, and relief after the tic is performed. Tics are common in children, with a prevalence of 6 to 12 percent. (See "Hyperkinetic movement disorders in children", section on 'Tic disorders'.)

Functional tics are challenging to diagnose, largely because nonfunctional tics have many of the same clinical characteristics. Many of the shared features that help differentiate FMD from other movement disorders (eg, sudden onset, distractibility, suggestibility, temporary remissions, and a fluctuating course) are also common clinical features of nonfunctional tics [86]. This may be why functional tics are rarely reported, accounting for only 2 percent of FMD [87].

An increase in functional tics has been observed during the coronavirus disease 2019 (COVID-19) pandemic [88,89]. Cases have been referred to as "TikTok tics," as affected individuals have commonly viewed online videos depicting tic-like behaviors. Most patients are females between 15 and 25 years of age [88]. Symptom onset is usually acute, with complex vocal and motor tics involving large-amplitude arm movements, self-injury, and a wide range of odd words or phrases, often with obscenities. Comorbid anxiety and depression are common.

Positive signs for functional tics include an inability to voluntarily suppress the movement, incomplete premonitory urge, and lack of fully stereotyped movements [86].

COMORBIDITIES — As a functional neurologic symptom disorder, FMD is highly comorbid with psychiatric, neurologic, and medical illnesses. Comorbidities are important to recognize as they may contribute to symptom genesis, perpetuation, and treatment response.

Patients have high rates of depression, generalized anxiety, panic, posttraumatic stress, and dissociative and somatoform symptom disorders. Personality disorders are also more common than in patients with neurologic disease, especially borderline, histrionic, and narcissistic types. (See "Conversion disorder in adults: Clinical features, assessment, and comorbidity", section on 'Psychiatric disorders'.)

Chronic pain, fatigue, anxiety, and cognitive symptoms are common in patients with FMD and occur at higher rates than formal psychiatric diagnoses [14,90]. Anxiety is especially common in patients with functional tremor but may not present overtly. Coexisting nonmotor functional symptoms, including functional seizures, sensory symptoms, visual symptoms, bladder changes, and irritable bowel symptoms, are also common. Comorbid movement disorders are diagnosed in approximately 15 to 25 percent of patients with FMD [8,91].

Some patients report prior suicidal ideation or suicide attempts [35,68], self-injurious behaviors [92], and psychiatric hospitalizations [35]. Increased harm avoidance and impulsivity, decreased novelty-seeking, self-directedness and active problem-solving, and external rather than internal locus of control have all been described in FMD [56-58]. Alexithymia, or difficulty recognizing emotion, has also been associated with FMD [35], but this remains controversial.

EVALUATION AND DIAGNOSIS — FMD is diagnosed clinically based upon characteristic clinical features and demonstration of positive signs (table 4). FMD should be suspected in patients with movements or postures that do not conform to usual characteristics of neurologic disorders; although psychiatric comorbidity is common, it is not always evident at the time of presentation and is not required for the diagnosis.

The diagnosis of FMD is best made by clinicians with expertise in movement disorders, including general neurologists [93]. An accurate diagnosis depends not only on the ability to recognize the characteristic features of FMD, but also on a strong knowledge of other movement disorders and their common and rare variants.

General principles

Rule-in, not rule-out – FMD is a "rule-in" diagnosis that requires the presence of characteristic clinical features (table 3) and the demonstration of positive signs (table 4) [94,95]. FMD is not a diagnosis of exclusion.

Comorbidity – Coexisting psychological factors and psychiatric disorders are not required for a diagnosis of FMD [3]. Pain, fatigue, and cognitive symptoms are common. FMD can coexist with other neurologic illness, including other movement disorders.

Role of investigations – Investigations should be done as appropriate to rule out comorbid neurologic disease. Laboratory-supported diagnoses with electrophysiology can be used in challenging cases of functional tremor or myoclonus. (See 'Electrodiagnostic testing' below.)

Rate of misdiagnosis Misdiagnosis is rare. A systematic review found that the misdiagnosis rate for patients with various functional symptoms, including some with abnormal movements, has been 4 percent since the 1970s [96]. While not specific for FMD, this finding suggests that the misdiagnosis rate is not unacceptably high compared with other psychiatric and neurologic disorders [97]. As an example, the misdiagnosis rate in Parkinson disease may be as high as 25 percent based on clinicopathologic studies [98].

Diagnostic criteria (DSM-5) — The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) classifies abnormal functional movements as a subtype of functional neurologic symptom disorder (conversion disorder) [1]. A DSM-5 diagnosis of conversion disorder requires symptoms of altered voluntary motor or sensory function, incompatibility with a recognized neurologic or general medical condition, lack of a better explanation, and the presence of significant distress or psychosocial impairment (table 1). (See "Conversion disorder in adults: Terminology, diagnosis, and differential diagnosis", section on 'Diagnosis'.)

History — History and direct observation are the core components of the diagnostic evaluation. Clinicians should ask about all of the following items, each of which is discussed in more detail separately (see "Conversion disorder in adults: Clinical features, assessment, and comorbidity", section on 'History'):

All current symptoms (neurologic, constitutional, psychological)

Circumstances at onset of symptoms (injury, illness, procedures)

Course of illness (duration, variability, triggers, alleviating factors, treatment trials)

Disability (physical, psychosocial, occupational)

Ideas, concerns, and expectations

Psychosocial functioning

Dissociation (feeling disconnected from oneself or the environment)

Family history (neurologic disorders, psychiatric disease, functional disorders)

Previous functional symptoms and disorders

Prior clinical experiences (misdiagnosis, iatrogenesis, excess tests and medication trials; often major source of mistrust and powerlessness)

Recent psychological stressors

Symptoms of comorbid psychiatric disorders

Examination and positive signs — Positive signs (table 4) are essential in diagnosing FMD [1]. Among functional neurologic symptom disorders, movement disorders are particularly amenable to positive signs on examination that aid the clinician to rule in a correct diagnosis. Demonstrating the positive sign to the patient is also an invaluable means of explaining the diagnosis, and it is useful when suggesting treatment approaches (See 'Education' below.)

The hallmark positive signs in FMD are variability and distractibility. These features apply to almost all FMD phenotypes. Additional positive signs specific to certain phenotypes are described above (see 'Clinical features' above) and listed in the table (table 4). Positive signs have shown a wide range of sensitivity (9 to 100 percent) but tighter range of specificity (64 to 100 percent) in functional motor and sensory symptom disorders, with 37 out of 41 signs having a specificity over 90 percent [72].

Distractibility — Distracting maneuvers temporarily diminish the intensity of FMD or suppress it entirely. By contrast, distracting maneuvers usually increase the intensity of abnormal movements in other movement disorders (such as dyskinesia in Parkinson disease).

Distraction techniques can be cognitive or motor and must be of sufficient difficulty to truly distract the patient.

Cognitive distractions – Examples include the history portion of the assessment, reciting the months of the year backward, listing animals, and generating words that begin with the same letter.

Motor distractions – Examples include the cranial nerve examination (ocular and oral movements are potent distractions if the functional movements do not involve the face), finger-counting in the contralateral hand, and asking the patient to draw letters or numbers on the floor with their foot. The distracting motor task must also be used in a part of the body not involved in the abnormal movement.

Distracting maneuvers may not be effective in longstanding FMD [99]. Fixed dystonia, functional myoclonus, and episodic or paroxysmal FMD are also less amenable to distraction. A corollary positive sign to distraction is when the symptom enhances when attention is drawn to it, either when the patient is describing it during the history, when it is pointed out by the examiner, or when the patient is engaging in a voluntary task that involves the body part with the symptom of concern (eg, writing in a patient with a functional dominant-hand tremor).

Variability — Variability is a core feature of FMD. Functional symptoms wax and wane over time. Variability can refer to the natural history of a symptom over time (by history) or at different points during the assessment. Functional movements may vary in terms of frequency, amplitude, direction, or location in the body.

Variation with body position is common in FMD. Seated findings may not correlate with the same findings while the patient is lying supine or walking. Findings may be different in the waiting room versus the clinic room.

Electrodiagnostic testing — Electrodiagnostic methods can provide additional supportive evidence for the diagnosis of functional tremor and functional myoclonus. However, electrodiagnostic methods for analyzing tremor and myoclonus require special expertise, are not universally available, and depend on patient effort for accuracy. They are not required or indicated in the majority of patients.

There are no definitive electrodiagnostic tests for distinguishing functional dystonia from other forms of dystonia [100].

Tremor analysis – Tremor analysis using surface electromyography (EMG) and accelerometry can identify features associated with functional tremor, including entrainment, coactivation of antagonist muscles, variability in tremor frequency, and increased tremor amplitude and frequency with weight-loading of the involved limb [23,43,99,101-103]. Coherence analysis is a quantitative method to determine the similarity of tremor oscillation frequency and phase in different limbs or body parts.

Functional tremor typically has the same frequency in different limbs or in the shaking limb and another limb performing distracting maneuvers [104]. Changes in frequency are simultaneous when they occur. By contrast, most other forms of tremor, including essential tremor and parkinsonian tremor, have similar but slightly different frequencies in different body parts, consistent with the presence of multiple oscillators [100].

Entrainment is a property whereby a tremor synchronizes with the frequency of voluntary tapping of another body part, most often the opposite hand. The degree of similarity of tremor frequency with voluntary tapping can be assessed by coherence analysis. Lack of entrainment suggests another etiology of tremor, since essential tremor and parkinsonian tremor maintain their original frequencies and do not entrain. However, in some cases functional tremor will stop or change frequency rather than show clear entrainment. [99].

Myoclonus analysis – Electrodiagnostic techniques, including surface EMG, electroencephalography (EEG), back-averaged EEG, and somatosensory evoked potentials, can be helpful in differentiating functional myoclonus from true myoclonus. Features associated with functional myoclonus on surface EMG include abnormally long and variable latency between the stimulus and the myoclonic jerk, variable patterns of muscle recruitment with each jerk, prolonged myoclonic burst duration, a triphasic pattern of agonist and antagonist muscle activation, and habituation with repeated stimulation [105,106].

In organic myoclonus of cortical origin, the myoclonic jerk has a short latency of 60 to 70 ms after a stimulus-induced cortical evoked potential on EEG and consists of short-duration (10 to 50 ms) burst activity in an agonist muscle on EMG accompanied by co-contraction in antagonist muscles. Brainstem myoclonus has short latencies (less than 80 ms) affecting the upper body. A pattern consistent with voluntary movement (ie, a long latency of 100 to 120 ms from stimulus to jerk) is suggestive of functional myoclonus. In addition, functional myoclonus is usually but not always preceded by a Bereitschaftspotential, which is a normal movement-related cognitive potential indicative of premotor activity that occurs prior to movement on back-averaged EEG [107].

Neuroimaging — Neuroimaging is usually obtained to exclude the possibility of a coexisting structural abnormality alongside FMD, such as demyelination or a compressive radiculopathy. The decision to image and the specific study should be based on clinical suspicion. Brain magnetic resonance imaging (MRI) is often the appropriate study, although a spine MRI may also be indicated for certain cases of myoclonus, dystonia, or tremor when symptoms involve a single limb. Care must be taken in explaining to patients why investigations are being done and to prepare the patient for potentially incidental findings.

Striatal dopamine transporter imaging using 123I-FP-CIT single-photon emission computed tomography (DaTscan) is not routinely indicated in the evaluation of FMD and is not specific for a functional cause. In a patient with parkinsonism, a normal DaTscan would be supportive of several diagnoses, including functional, drug-induced, or vascular parkinsonism [85]. In addition, a change from normal to abnormal may occur over time, and, therefore, a single test should not be used to support a diagnosis of FMD. (See "Diagnosis and differential diagnosis of Parkinson disease", section on 'DaTscan'.)

Differential diagnosis — An accurate diagnosis of FMD depends on strong knowledge of other movement disorders and their common and rare variants. Movement disorders that may be confused with functional movements vary based on the particular movement and are discussed above. (See 'Clinical features' above.)

The differential diagnosis of functional neurologic symptom disorder also includes psychiatric disorders, including somatic symptom disorder, depersonalization/derealization disorder, feigned symptoms, factious disorder, and malingering. The distinction between these disorders and functional disorders is reviewed separately. (See "Conversion disorder in adults: Terminology, diagnosis, and differential diagnosis", section on 'Differential diagnosis'.)

TREATMENT — Treatment of FMD follows the same principles of therapy as for functional neurologic symptom disorder. Treatment should be individualized and follow a stepped model of care based on symptom severity and complexity to optimize resource allocation [108].

Step 1 – All patients should be provided with a diagnosis, education, and advice by a neurologist as first-line therapy. (See 'Delivering the diagnosis' below and 'Education' below.)

Step 2 – Patients with more severe symptoms but without complex psychiatric comorbidities may benefit from a brief rehabilitation intervention with a physical, occupational, or speech therapist, with or without accompanying psychotherapy. (See 'Motor retraining' below and 'Psychological therapies' below.)

Step 3 – Patients with complex symptom presentations, those with a high level of disability and comorbidities, and those who have failed prior treatment interventions may require specialized multidisciplinary therapy delivered in an outpatient, day hospital, or inpatient setting [109]. (See 'Multidisciplinary therapies' below and 'Refractory/chronic disease' below.)

Delivering the diagnosis — The first line of treatment consists of disclosing the diagnosis to the patient. Clinicians should demonstrate the rationale for the diagnosis of FMD, show the patient their positive signs, and convey recovery potential.

It should be emphasized that the problem is not "made up" by the patient or "in their head," and that FMD is a real and common condition. It is important to take the patient's complaints seriously. Some patients with FMD will have had prior negative experiences with health care providers, and inquiring about these instances while also validating the patient's symptom complex can help build rapport and engagement [11]. Importantly, some patients will improve with a well-delivered diagnosis alone.

A roadmap for presenting the diagnosis is reviewed in more detail separately. (See "Conversion disorder in adults: Treatment", section on 'Presenting the diagnosis'.)

Education — Patients should be directed to reliable sources of information about FMD. Some neurologists find it useful to review symptoms with the patient using a website, FND Guide, which presents balanced information about functional neurologic symptom disorders including FMD.

Demonstration – Showing the patient their positive signs is a valuable way to help the patient agree with and understand the diagnosis, particularly in movement disorders [110]. For example, demonstrating to the patient that their tremor temporarily resolves when they tap the fingers of their other hand shows them not only that distraction improves the tremor, but also that their nervous system is capable of functioning normally at times.

Entrainment – Entrainment can be used as a therapeutic strategy at the time of diagnosis at the bedside to show the patient that they can retrain the tremor frequency and reduce the tremor severity (ie, "self-entrain") [111]. This tends to be most useful for unilateral functional hand tremor. The contralateral hand taps the leg at a fast frequency that matches the frequency of the tremor. The patient then deliberately slows down the frequency until it stops, and the entrained hand also stops.

Use of analogies – Explaining the diagnosis can be made easier through the use of analogies, such as a "hardware versus software" problem, or abnormal motor programs learned by the brain.

Motor retraining — For most patients who do not improve with education alone, we suggest specialized rehabilitation, which can be delivered by physiotherapists [112], occupational therapists [113], or speech therapists [114], depending on the movement disorder.

Eligibility and barriers – Prior to embarking on therapy, it is important to determine if any barriers to rehabilitation are present, such as severe pain or fatigue, diagnostic disagreement or alternate illness beliefs, or ongoing psychosocial stressors that will limit engagement [11].

It is also important that the symptoms of concern to the patient (and not just the provider) are amenable to physiotherapy. For example, gait disorders or tremor that are present more or less constantly are more amenable to rehabilitation than episodic generalized dystonia, in which the symptoms are only intermittently present, or fixed dystonia, in which there is little to no variability present.

Therapeutic principles – The principles of motor-retraining physiotherapy differ markedly from standard neurorehabilitation; thus, working with a therapist with experience in these techniques is essential. Therapy is delivered within a psychologically informed framework, and relaxation and mindfulness training are incorporated into treatment sessions. FMD-specific therapy principles include [112-115]:

Address function, such as transfers and walking, rather than impairments such as weakness

Divert attention away from abnormal movements

Notice symptom variability

Use energy/activity rationing, also called pacing

Limit "hands-on" treatment

Facilitate rather than support movements

Encourage early weight-bearing

Use a goal-directed approach focused on function and automatic movement

Minimize reinforcement of maladaptive movement patterns and postures

Avoid adaptive equipment and mobility aids

Efficacy – There is now a good evidence base for physiotherapy for FMD, including several small randomized trials [112,116-118].

A randomized trial compared three weeks of inpatient physical therapy (including education) with a waiting list control condition in hospitalized patients with psychogenic gait disorder (n = 60) [117]. Ambulation and functional independence improved significantly more with physical therapy, the clinical effect was large, and the benefits were maintained at one-year follow-up.

A second randomized trial compared a five-day intensive outpatient specialized physical therapy program with standard neurologic physical therapy in 60 patients with functional motor disorders [119]. The control group received an average of five sessions. At six-month follow-up, improvement occurred in four times as many patients in the intervention group than the controls (72 versus 18 percent).

Psychological therapies — Psychiatric interventions are individualized according to the underlying psychiatric diagnosis and best accomplished by involvement with a psychiatrist or psychologist who is familiar with FMD.

Patients may decline psychotherapy because they refuse to accept that "talking" treatments can be beneficial for physical symptoms. This concern can often be addressed by delivering psychotherapy as part of medical care, validating the patient's experience and symptoms as not being "all in their head," and using integrated care models with partnerships between neurology and psychiatry [120,121]. In some cases, pharmacotherapy may be useful for comorbid, active psychiatric concerns such as depression or anxiety [122]. (See "Conversion disorder in adults: Treatment", section on 'Pharmacotherapy'.)

In FMD, psychotherapy can be effective either in conjunction with motor retraining or delivered sequentially [123-126]. As an example, functional tremor with accompanying anxiety can be treated with motor retraining physio- or occupational therapy to target tremor, in concert with cognitive-behavioral therapy (CBT) to target unhelpful thought patterns and anxiety. One study in 15 patients with functional tremor showed complete remission at 12 weeks in 73 percent of the cohort following a course of CBT alone [126]. (See "Conversion disorder in adults: Treatment", section on 'Cognitive-behavioral therapy'.)

Psychodynamic psychotherapy has a good evidence base in functional neurologic symptom disorder. Studies in FMD are more limited, but there may be a role for individual psychotherapy with or without pharmacotherapy [127]. (See "Conversion disorder in adults: Treatment".)

Multidisciplinary therapies — Patients with complex symptom presentations, those with a high level of disability and comorbidities, and those who have failed prior treatment interventions are likely to benefit from specialized multidisciplinary therapy delivered in an outpatient, day hospital, or inpatient setting.

Inpatient programs for severe FMD cases have shown good clinical outcomes in observational studies [7,128-132]. As an example, a prospective observational study assessed patients (n = 66) who were hospitalized on a specialist unit for severe conversion disorder (mixed subtype) and received a four-week multidisciplinary program that included physical therapy, occupational therapy, CBT, neuropsychiatry assessment, and neurology input as required. Improvement of psychiatric symptoms, behavior, and functioning at discharge was significant and clinically large, according to clinician ratings [132]. General health was rated as "better" or "much better" by 66 percent of patients, both at discharge and the one-year follow-up assessment.

Complex patients are more resource intensive and require specialized outpatient care as well. Such patients may benefit from dedicated functional neurologic symptom disorder clinics where access to adjunctive treatments is available [90], such as chronic pain programs, long-term psychotherapy, trauma therapy, and other therapies for non-movement-related functional symptoms such as vestibular therapy.

Other therapies have been investigated in FMD and include transcranial magnetic stimulation [133] and hypnosis [123,134]. (See "Conversion disorder in adults: Treatment", section on 'Third line treatment'.)

Refractory/chronic disease — A proportion of patients will not respond to treatment and develop chronic FMD. It should be recognized that the absence of a structural lesion is not indicative of reversibility of the functional syndrome.

Chronic FMD can occur for several reasons, including internal and external factors related to the patient and the health care team. Misdiagnosis and unrecognized comorbidities should always be considered when patients fail to respond to standard therapies. (See "Conversion disorder in adults: Treatment", section on 'Persistently ill patients'.)

In patients with chronic FMD, treatment may consist of periodic reassessments to ascertain readiness to engage in treatment, reassurance around new symptoms, and prevention of iatrogenic harm from diagnostic tests or surgical procedures. Persistently ill patients should generally be treated by primary care clinicians with a conservative approach, along the lines of prophylactic management models used in somatization disorder. (See "Somatic symptom disorder: Treatment", section on 'Treatment-refractory patients'.)

Identifying who may or may not respond to therapy upfront and triaging to appropriate treatments are important for resource allocation, given the prevalence of these disorders and the high health care utilization of this portion of the population.

PROGNOSIS — Prognosis for functional neurologic symptom disorder as a whole is guarded, and many patients face long-term symptoms and disability. Across subtypes, patients with sensory symptoms tend to do better than those with weakness/paralysis and FMD. (See "Conversion disorder in adults: Epidemiology, pathogenesis, and prognosis", section on 'Prognosis'.)

In a systematic review of FMD that identified 24 studies in 2069 patients, 40 percent of patients had the same or worse outcome with a median follow-up of 7.4 years, and only 20 percent of patients experienced complete remission [135]. Among phenotypes, functional dystonia had the worst prognosis, with nearly 80 percent of patients having the same or worse symptoms over time [135,136]. Functional tremor also has a relatively poor prognosis, with 44 to 90 percent of patients the same or worse at follow-up [18,43,137,138]. An important limitation is that most prognostic studies have been in untreated cohorts.

Baseline predictors of outcome in patients with FMD are similar to those in patients with other subtypes of functional neurologic symptom disorder (table 4). There is conflicting evidence regarding the correlation of prognosis with pending litigation, age, comorbid anxiety and depression, intelligence quotient, educational status, and marital status [135]. The interpretation of most prognostic studies is hampered because patients with functional symptoms were not compared with controls with recognizable neurologic disease.

FMD often occurs in midlife, and the socioeconomic impact is notable. Patients with FMD show comparable rates of disability to those seen in other neurologic diseases, though with increased rates of total symptom burden and mental distress [139,140]. Unemployment rates range from 23 to 84 percent, and the reported percentage of patients who are receiving or seeking medical disability has ranged from 24 to 55 percent [11]. One multicenter study of FMD from Canada, the United Kingdom, and Switzerland found that 35 percent of patients were not working because of ill health, 26 percent were receiving disability benefits, and 10 to 38 percent required a care provider for daily activities [90].

SUMMARY AND RECOMMENDATIONS

Definition – Functional movement disorder (FMD) is a subtype of functional neurologic symptom disorder (conversion disorder) defined by abnormal movements that occur as a result of abnormal functioning of the nervous system, incongruent with known movement disorders. (See 'Introduction' above and 'Terminology' above.)

Epidemiology – FMD accounts for 2 to 10 percent of all movement disorders. Functional tremor is the most frequent phenotype of FMD, followed by functional dystonia. Mixed FMD with more than one phenotype is common. (See 'Epidemiology' above.)

Etiology – FMD is best conceptualized using a biopsychosocial model of predisposing, precipitating, and perpetuating factors. Factors can be biologic, psychological, or social, and the combination of factors is unique to each patient (table 2). (See 'Etiologic factors' above and 'Pathogenesis' above.)

Clinical features – FMD often begins abruptly after illness or injury, has a fast progression to disability, and is associated with variable symptoms that wax and wane over time (table 3). Symptoms usually improve with distraction and worsen with attention. (See 'Shared features' above.)

The main FMD syndromes are functional tremor, functional dystonia, functional gait, functional myoclonus, and functional parkinsonism. Each is associated with distinctive clinical features and positive signs that help distinguish FMD from other movement disorders (table 4). (See 'Functional tremor' above and 'Functional dystonia' above and 'Functional gait' above and 'Functional myoclonus' above and 'Functional parkinsonism' above and 'Functional tics' above.)

Diagnosis – FMD is a rule-in diagnosis and not a diagnosis of exclusion, and follow-up is required as clinically indicated. Accurate diagnosis is based on the entire clinical picture and demonstration of positive signs on examination. Coexisting psychological factors and psychiatric disorders are common but not required. (See 'Evaluation and diagnosis' above.)

Laboratory-supported diagnosis can be achieved in challenging cases of tremor or myoclonus using electrodiagnostic studies, such as electromyography (EMG) and electroencephalography (EEG). Neuroimaging has a role when there is clinical suspicion for a coexisting structural abnormality alongside FMD. (See 'Electrodiagnostic testing' above and 'Neuroimaging' above.)

Treatment – Optimal management of FMD consists of early diagnosis and individualized treatment depending on symptom severity and syndrome complexity. There is no "one size fits all" treatment. (See 'Treatment' above.)

Treatment begins with diagnosis delivery. Clinicians should emphasize the rationale for the diagnosis, demonstrate to the patient their positive signs, convey the potential for reversibility, and provide educational resources, such as FND Guide. (See 'Delivering the diagnosis' above and 'Education' above.)

Patients who do not improve with diagnosis and education alone are offered motor retraining physiotherapy, occupational therapy, or speech therapy. (See 'Motor retraining' above.)

Psychological therapies such as cognitive behavioral therapy can be effective adjuncts to physical therapy, either together or in sequence. (See 'Psychological therapies' above.)

Multidisciplinary rehabilitation in either in- or outpatient models may be required for more complex, longstanding, and/or highly disabled patients. (See 'Multidisciplinary therapies' above.)

Some patients may not improve with therapy. Management of chronic FMD should center around minimization of iatrogenic harm. (See 'Refractory/chronic disease' above.)

Prognosis – Prognosis for FMD is generally unfavorable in untreated cohorts. Factors associated with a more favorable prognosis include short duration of symptoms, early diagnosis, and good therapeutic alliance with the clinician. (See 'Prognosis' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Janis M Miyasaki, MD, MEd, who contributed to an earlier version of this topic review.

REFERENCES

  1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 5th ed, American Psychiatric Association, Arlington 2013.
  2. World Health Organization. International Classification of Diseases, 11th Revision (ICD-11). https://www.who.int/classifications/classification-of-diseases (Accessed on October 29, 2021).
  3. Williams DT, Ford B, Fahn S. Phenomenology and psychopathology related to psychogenic movement disorders. Adv Neurol 1995; 65:231.
  4. Factor SA, Podskalny GD, Molho ES. Psychogenic movement disorders: frequency, clinical profile, and characteristics. J Neurol Neurosurg Psychiatry 1995; 59:406.
  5. Schwingenschuh P, Pont-Sunyer C, Surtees R, et al. Psychogenic movement disorders in children: a report of 15 cases and a review of the literature. Mov Disord 2008; 23:1882.
  6. Park JE. Clinical Characteristics of Functional Movement Disorders: A Clinic-based Study. Tremor Other Hyperkinet Mov (N Y) 2018; 8:504.
  7. Schrag A, Trimble M, Quinn N, Bhatia K. The syndrome of fixed dystonia: an evaluation of 103 patients. Brain 2004; 127:2360.
  8. Kirsch DB, Mink JW. Psychogenic movement disorders in children. Pediatr Neurol 2004; 30:1.
  9. Chouksey A, Pandey S. Functional Movement Disorders in Elderly. Tremor Other Hyperkinet Mov (N Y) 2019; 9.
  10. Batla A, Stamelou M, Edwards MJ, et al. Functional movement disorders are not uncommon in the elderly. Mov Disord 2013; 28:540.
  11. Perez DL, Aybek S, Popkirov S, et al. A Review and Expert Opinion on the Neuropsychiatric Assessment of Motor Functional Neurological Disorders. J Neuropsychiatry Clin Neurosci 2021; 33:14.
  12. Ani C, Reading R, Lynn R, et al. Incidence and 12-month outcome of non-transient childhood conversion disorder in the U.K. and Ireland. Br J Psychiatry 2013; 202:413.
  13. Stephen CD, Fung V, Lungu CI, Espay AJ. Assessment of Emergency Department and Inpatient Use and Costs in Adult and Pediatric Functional Neurological Disorders. JAMA Neurol 2021; 78:88.
  14. Tinazzi M, Morgante F, Marcuzzo E, et al. Clinical Correlates of Functional Motor Disorders: An Italian Multicenter Study. Mov Disord Clin Pract 2020; 7:920.
  15. Cubo E, Hinson VK, Goetz CG, et al. Transcultural comparison of psychogenic movement disorders. Mov Disord 2005; 20:1343.
  16. Miyasaki J. Unpublished data, Morton and Gloria Shulman Movement Disorders Centre, Toronto Western Hospital, Univeristy of Toronto.
  17. Bhatia KP, Schneider SA. Psychogenic tremor and related disorders. J Neurol 2007; 254:569.
  18. McKeon A, Ahlskog JE, Bower JH, et al. Psychogenic tremor: long-term prognosis in patients with electrophysiologically confirmed disease. Mov Disord 2009; 24:72.
  19. Ludwig L, Pasman JA, Nicholson T, et al. Stressful life events and maltreatment in conversion (functional neurological) disorder: systematic review and meta-analysis of case-control studies. Lancet Psychiatry 2018; 5:307.
  20. Binzer M, Kullgren G. Motor conversion disorder. A prospective 2- to 5-year follow-up study. Psychosomatics 1998; 39:519.
  21. Feinstein A, Stergiopoulos V, Fine J, Lang AE. Psychiatric outcome in patients with a psychogenic movement disorder: a prospective study. Neuropsychiatry Neuropsychol Behav Neurol 2001; 14:169.
  22. Kranick S, Ekanayake V, Martinez V, et al. Psychopathology and psychogenic movement disorders. Mov Disord 2011; 26:1844.
  23. Hinson VK, Haren WB. Psychogenic movement disorders. Lancet Neurol 2006; 5:695.
  24. Thomas M, Vuong KD, Jankovic J. Long-term prognosis of patients with psychogenic movement disorders. Parkinsonism Relat Disord 2006; 12:382.
  25. Pareés I, Kojovic M, Pires C, et al. Physical precipitating factors in functional movement disorders. J Neurol Sci 2014; 338:174.
  26. O'Connell N, Nicholson TR, Wessely S, David AS. Characteristics of patients with motor functional neurological disorder in a large UK mental health service: a case-control study. Psychol Med 2020; 50:446.
  27. Defazio G, Pastore A, Pellicciari R, et al. Personality disorders and somatization in functional and organic movement disorders. Psychiatry Res 2017; 257:227.
  28. Peckham EL, Hallett M. Psychogenic movement disorders. Neurol Clin 2009; 27:801.
  29. LaFaver K, Hallett M. Functional or psychogenic: what's the better name? Mov Disord 2014; 29:1698.
  30. Simon DK, Nishino S, Scammell TE. Mistaken diagnosis of psychogenic gait disorder in a man with status cataplecticus ("limp man syndrome"). Mov Disord 2004; 19:838.
  31. Edwards MJ, Stone J, Lang AE. Functional/psychogenic movement disorders: do we know what they are? Mov Disord 2014; 29:1696.
  32. Edwards MJ, Fotopoulou A, Pareés I. Neurobiology of functional (psychogenic) movement disorders. Curr Opin Neurol 2013; 26:442.
  33. Edwards MJ, Adams RA, Brown H, et al. A Bayesian account of 'hysteria'. Brain 2012; 135:3495.
  34. Pareés I, Brown H, Nuruki A, et al. Loss of sensory attenuation in patients with functional (psychogenic) movement disorders. Brain 2014; 137:2916.
  35. Demartini B, Petrochilos P, Ricciardi L, et al. The role of alexithymia in the development of functional motor symptoms (conversion disorder). J Neurol Neurosurg Psychiatry 2014; 85:1132.
  36. Newby R, Alty J, Kempster P. Functional dystonia and the borderland between neurology and psychiatry: New concepts. Mov Disord 2016; 31:1777.
  37. Maurer CW, LaFaver K, Ameli R, et al. Impaired self-agency in functional movement disorders: A resting-state fMRI study. Neurology 2016; 87:564.
  38. Huys AML, Haggard P, Bhatia KP, Edwards MJ. Misdirected attentional focus in functional tremor. Brain 2021; 144:3436.
  39. Maurer CW, LaFaver K, Limachia GS, et al. Gray matter differences in patients with functional movement disorders. Neurology 2018; 91:e1870.
  40. Suchowersky O, 2006, personal communication.
  41. Edwards MJ, Bhatia KP, Cordivari C. Immediate response to botulinum toxin injections in patients with fixed dystonia. Mov Disord 2011; 26:917.
  42. Thomas M, Jankovic J. Psychogenic movement disorders: diagnosis and management. CNS Drugs 2004; 18:437.
  43. Deuschl G, Köster B, Lücking CH, Scheidt C. Diagnostic and pathophysiological aspects of psychogenic tremors. Mov Disord 1998; 13:294.
  44. Lidstone SC, Lang AE. How Do I Examine Patients With Functional Tremor? Mov Disord Clin Pract 2020; 7:587.
  45. Simons RC. The resolution of the Latah paradox. J Nerv Ment Dis 1980; 168:195.
  46. Park JE, Maurer CW, Hallett M. The "Whack-a-Mole" Sign in Functional Movement Disorders. Mov Disord Clin Pract 2015; 2:286.
  47. Brown P, Rothwell JC, Thompson PD, et al. The hyperekplexias and their relationship to the normal startle reflex. Brain 1991; 114 ( Pt 4):1903.
  48. van der Stouwe AM, Elting JW, van der Hoeven JH, et al. How typical are 'typical' tremor characteristics? Sensitivity and specificity of five tremor phenomena. Parkinsonism Relat Disord 2016; 30:23.
  49. Sa DS, Mailis-Gagnon A, Nicholson K, Lang AE. Posttraumatic painful torticollis. Mov Disord 2003; 18:1482.
  50. Hawley JS, Weiner WJ. Psychogenic dystonia and peripheral trauma. Neurology 2011; 77:496.
  51. Tarsy D. Comparison of acute- and delayed-onset posttraumatic cervical dystonia. Mov Disord 1998; 13:481.
  52. Bhatia KP, Bhatt MH, Marsden CD. The causalgia-dystonia syndrome. Brain 1993; 116 ( Pt 4):843.
  53. Lang AE, Chen R. Dystonia in complex regional pain syndrome type I. Ann Neurol 2010; 67:412.
  54. Majumdar A, López-Casas J, Poo P, et al. Syndrome of fixed dystonia in adolescents--short term outcome in 4 cases. Eur J Paediatr Neurol 2009; 13:466.
  55. Sankhla C, Lai EC, Jankovic J. Peripherally induced oromandibular dystonia. J Neurol Neurosurg Psychiatry 1998; 65:722.
  56. Jankovic J. Can peripheral trauma induce dystonia and other movement disorders? Yes! Mov Disord 2001; 16:7.
  57. Weiner WJ. Can peripheral trauma induce dystonia? No! Mov Disord 2001; 16:13.
  58. Carroll CG, Hawley JS, Ney JP. Post-traumatic shoulder dystonia in an active duty soldier. Mil Med 2006; 171:494.
  59. Bohlhalter S, Leon-Sarmiento FE, Hallett M. Abnormality of motor cortex excitability in peripherally induced dystonia. Mov Disord 2007; 22:1186.
  60. Kumar H, Jog M. Peripheral trauma induced dystonia or post-traumatic syndrome? Can J Neurol Sci 2011; 38:22.
  61. Munts AG, Koehler PJ. How psychogenic is dystonia? Views from past to present. Brain 2010; 133:1552.
  62. van Rooijen DE, Geraedts EJ, Marinus J, et al. Peripheral trauma and movement disorders: a systematic review of reported cases. J Neurol Neurosurg Psychiatry 2011; 82:892.
  63. Fasano A, Valadas A, Bhatia KP, et al. Psychogenic facial movement disorders: clinical features and associated conditions. Mov Disord 2012; 27:1544.
  64. Kanaan RAA, Duncan R, Goldstein LH, et al. Are psychogenic non-epileptic seizures just another symptom of conversion disorder? J Neurol Neurosurg Psychiatry 2017; 88:425.
  65. Baik JS, Lang AE. Gait abnormalities in psychogenic movement disorders. Mov Disord 2007; 22:395.
  66. Lempert T, Brandt T, Dieterich M, Huppert D. How to identify psychogenic disorders of stance and gait. A video study in 37 patients. J Neurol 1991; 238:140.
  67. Okun MS, Koehler PJ. Paul Blocq and (psychogenic) astasia abasia. Mov Disord 2007; 22:1373.
  68. Sudarsky L. Psychogenic gait disorders. Semin Neurol 2006; 26:351.
  69. Keane JR. Hysterical gait disorders: 60 cases. Neurology 1989; 39:586.
  70. Nutt JG, Marsden CD, Thompson PD. Human walking and higher-level gait disorders, particularly in the elderly. Neurology 1993; 43:268.
  71. Lidstone SC, Araújo R, Stone J, Bloem BR. Ten myths about functional neurological disorder. Eur J Neurol 2020; 27:e62.
  72. Daum C, Gheorghita F, Spatola M, et al. Interobserver agreement and validity of bedside 'positive signs' for functional weakness, sensory and gait disorders in conversion disorder: a pilot study. J Neurol Neurosurg Psychiatry 2015; 86:425.
  73. Laub HN, Dwivedi AK, Revilla FJ, et al. Diagnostic performance of the "Huffing and Puffing" sign in psychogenic (functional) movement disorders. Mov Disord Clin Pract 2015; 2:29.
  74. Jordbru AA, Smedstad LM, Moen VP, Martinsen EW. Identifying patterns of psychogenic gait by video-recording. J Rehabil Med 2012; 44:31.
  75. Okun MS, Rodriguez RL, Foote KD, Fernandez HH. The "chair test" to aid in the diagnosis of psychogenic gait disorders. Neurologist 2007; 13:87.
  76. van der Salm SM, Erro R, Cordivari C, et al. Propriospinal myoclonus: clinical reappraisal and review of literature. Neurology 2014; 83:1862.
  77. Monday K, Jankovic J. Psychogenic myoclonus. Neurology 1993; 43:349.
  78. Sa DS, Galvez-Jimenez N, Lang AE. Psychogenic movement disorders. In: Movement Disorders, 3rd ed, Watts RL, Standaert DG, Obeso JA (Eds), McGraw-Hill, New York 2012. p.975.
  79. Benaderette S, Zanotti Fregonara P, Apartis E, et al. Psychogenic parkinsonism: a combination of clinical, electrophysiological, and [(123)I]-FP-CIT SPECT scan explorations improves diagnostic accuracy. Mov Disord 2006; 21:310.
  80. Miyasaki JM, Sa DS, Galvez-Jimenez N, Lang AE. Psychogenic movement disorders. Can J Neurol Sci 2003; 30 Suppl 1:S94.
  81. Lang AE, Koller WC, Fahn S. Psychogenic parkinsonism. Arch Neurol 1995; 52:802.
  82. Jankovic J. Diagnosis and treatment of psychogenic parkinsonism. J Neurol Neurosurg Psychiatry 2011; 82:1300.
  83. Onofrj M, Bonanni L, Manzoli L, Thomas A. Cohort study on somatoform disorders in Parkinson disease and dementia with Lewy bodies. Neurology 2010; 74:1598.
  84. Hallett M. Psychogenic parkinsonism. J Neurol Sci 2011; 310:163.
  85. Kägi G, Bhatia KP, Tolosa E. The role of DAT-SPECT in movement disorders. J Neurol Neurosurg Psychiatry 2010; 81:5.
  86. Demartini B, Ricciardi L, Parees I, et al. A positive diagnosis of functional (psychogenic) tics. Eur J Neurol 2015; 22:527.
  87. Lang AE. General overview of psychogenic movement disorders: Epidemiology, diagnosis, and prognosis. In: Psychogenic Movement Disorders; Neurology and Neuropsychiatry, Hallet M, Fahn S, Jankovic J, et al (Eds), Lippincott Williams & Wilkins, Philadelphia 2006. p.35.
  88. Pringsheim T, Ganos C, McGuire JF, et al. Rapid Onset Functional Tic-Like Behaviors in Young Females During the COVID-19 Pandemic. Mov Disord 2021; 36:2707.
  89. Müller-Vahl KR, Edwards MJ. Mind the Difference Between Primary Tics and Functional Tic-like Behaviors. Mov Disord 2021; 36:2716.
  90. Aybek S, Lidstone SC, Nielsen G, et al. What Is the Role of a Specialist Assessment Clinic for FND? Lessons From Three National Referral Centers. J Neuropsychiatry Clin Neurosci 2020; 32:79.
  91. Ganos C, Aguirregomozcorta M, Batla A, et al. Psychogenic paroxysmal movement disorders--clinical features and diagnostic clues. Parkinsonism Relat Disord 2014; 20:41.
  92. Jankovic J. "Psychogenic" versus "functional" movement disorders? That is the question. Mov Disord 2014; 29:1697.
  93. van der Salm SM, van Rootselaar AF, Cath DC, et al. Clinical decision-making in functional and hyperkinetic movement disorders. Neurology 2017; 88:118.
  94. Gupta A, Lang AE. Psychogenic movement disorders. Curr Opin Neurol 2009; 22:430.
  95. Lang AE, Voon V. Psychogenic movement disorders: past developments, current status, and future directions. Mov Disord 2011; 26:1175.
  96. Stone J, Smyth R, Carson A, et al. Systematic review of misdiagnosis of conversion symptoms and "hysteria". BMJ 2005; 331:989.
  97. Voon V, Lang AE, Hallett M. Diagnosing psychogenic movement disorders-which criteria should be used in clinical practice? Nat Clin Pract Neurol 2007; 3:134.
  98. Tolosa E, Wenning G, Poewe W. The diagnosis of Parkinson's disease. Lancet Neurol 2006; 5:75.
  99. McAuley J, Rothwell J. Identification of psychogenic, dystonic, and other organic tremors by a coherence entrainment test. Mov Disord 2004; 19:253.
  100. Hallett M. Physiology of psychogenic movement disorders. J Clin Neurosci 2010; 17:959.
  101. Raethjen J, Kopper F, Govindan RB, et al. Two different pathogenetic mechanisms in psychogenic tremor. Neurology 2004; 63:812.
  102. Schwingenschuh P, Katschnig P, Seiler S, et al. Moving toward "laboratory-supported" criteria for psychogenic tremor. Mov Disord 2011; 26:2509.
  103. Schwingenschuh P, Saifee TA, Katschnig-Winter P, et al. Validation of "laboratory-supported" criteria for functional (psychogenic) tremor. Mov Disord 2016; 31:555.
  104. O'Suilleabhain PE, Matsumoto JY. Time-frequency analysis of tremors. Brain 1998; 121 ( Pt 11):2127.
  105. Thompson PD, Colebatch JG, Brown P, et al. Voluntary stimulus-sensitive jerks and jumps mimicking myoclonus or pathological startle syndromes. Mov Disord 1992; 7:257.
  106. Brown P, Thompson PD. Electrophysiological aids to the diagnosis of psychogenic jerks, spasms, and tremor. Mov Disord 2001; 16:595.
  107. Shibasaki H, Hallett M. What is the Bereitschaftspotential? Clin Neurophysiol 2006; 117:2341.
  108. Stepped care for functional neurological symptoms. Healthcare Improvement Scotland. NHS Scotland. Available at: http://healthcareimprovementscotland.org/idoc.ashx?docid=6d302668-ff12-4f53-b547-72c19531e37a&version=-1 (Accessed on November 05, 2021).
  109. LaFaver K, LaFrance WC, Price ME, et al. Treatment of functional neurological disorder: current state, future directions, and a research agenda. CNS Spectr 2020; :1.
  110. Stone J, Edwards M. Trick or treat? Showing patients with functional (psychogenic) motor symptoms their physical signs. Neurology 2012; 79:282.
  111. Espay AJ, Edwards MJ, Oggioni GD, et al. Tremor retrainment as therapeutic strategy in psychogenic (functional) tremor. Parkinsonism Relat Disord 2014; 20:647.
  112. Nielsen G, Stone J, Matthews A, et al. Physiotherapy for functional motor disorders: a consensus recommendation. J Neurol Neurosurg Psychiatry 2015; 86:1113.
  113. Nicholson C, Edwards MJ, Carson AJ, et al. Occupational therapy consensus recommendations for functional neurological disorder. J Neurol Neurosurg Psychiatry 2020; 91:1037.
  114. Baker J, Barnett C, Cavalli L, et al. Management of functional communication, swallowing, cough and related disorders: consensus recommendations for speech and language therapy. J Neurol Neurosurg Psychiatry 2021; 92:1112.
  115. Edwards MJ, Stone J, Nielsen G. Physiotherapists and patients with functional (psychogenic) motor symptoms: a survey of attitudes and interest. J Neurol Neurosurg Psychiatry 2012; 83:655.
  116. Czarnecki K, Thompson JM, Seime R, et al. Functional movement disorders: successful treatment with a physical therapy rehabilitation protocol. Parkinsonism Relat Disord 2012; 18:247.
  117. Jordbru AA, Smedstad LM, Klungsøyr O, Martinsen EW. Psychogenic gait disorder: a randomized controlled trial of physical rehabilitation with one-year follow-up. J Rehabil Med 2014; 46:181.
  118. Nielsen G, Ricciardi L, Demartini B, et al. Outcomes of a 5-day physiotherapy programme for functional (psychogenic) motor disorders. J Neurol 2015; 262:674.
  119. Nielsen G, Buszewicz M, Stevenson F, et al. Randomised feasibility study of physiotherapy for patients with functional motor symptoms. J Neurol Neurosurg Psychiatry 2017; 88:484.
  120. Lidstone SC, MacGillivray L, Lang AE. Integrated Therapy for Functional Movement Disorders: Time for a Change. Mov Disord Clin Pract 2020; 7:169.
  121. Lidstone SC, Nassif W, Juncos J, et al. Diagnosing functional neurological disorder: seeing the whole picture. CNS Spectr 2020; :1.
  122. Voon V, Lang AE. Antidepressant treatment outcomes of psychogenic movement disorder. J Clin Psychiatry 2005; 66:1529.
  123. Ricciardi L, Edwards MJ. Treatment of functional (psychogenic) movement disorders. Neurotherapeutics 2014; 11:201.
  124. Shapiro AP, Teasell RW. Behavioural interventions in the rehabilitation of acute v. chronic non-organic (conversion/factitious) motor disorders. Br J Psychiatry 2004; 185:140.
  125. Vizcarra JA, Lopez-Castellanos JR, Dwivedi AK, et al. OnabotulinumtoxinA and cognitive behavioral therapy in functional dystonia: A pilot randomized clinical trial. Parkinsonism Relat Disord 2019; 63:174.
  126. Espay AJ, Ries S, Maloney T, et al. Clinical and neural responses to cognitive behavioral therapy for functional tremor. Neurology 2019; 93:e1787.
  127. Hinson VK, Weinstein S, Bernard B, et al. Single-blind clinical trial of psychotherapy for treatment of psychogenic movement disorders. Parkinsonism Relat Disord 2006; 12:177.
  128. Rosebush P, Mazurek M. Treatment of conversion disorder. In: Psychogenic Movement Disorders, Hallett M, Fahn S, Jankovic J, et al (Eds), Lippincott Williams & Wilkins, Philadelphia 2006. p.289.
  129. Jacob AE, Kaelin DL, Roach AR, et al. Motor Retraining (MoRe) for Functional Movement Disorders: Outcomes From a 1-Week Multidisciplinary Rehabilitation Program. PM R 2018; 10:1164.
  130. McCormack R, Moriarty J, Mellers JD, et al. Specialist inpatient treatment for severe motor conversion disorder: a retrospective comparative study. J Neurol Neurosurg Psychiatry 2014; 85:895.
  131. Saifee TA, Kassavetis P, Pareés I, et al. Inpatient treatment of functional motor symptoms: a long-term follow-up study. J Neurol 2012; 259:1958.
  132. Demartini B, Batla A, Petrochilos P, et al. Multidisciplinary treatment for functional neurological symptoms: a prospective study. J Neurol 2014; 261:2370.
  133. Oriuwa C, Mollica A, Feinstein A, et al. Neuromodulation for the treatment of functional neurological disorder and somatic symptom disorder: a systematic review. J Neurol Neurosurg Psychiatry 2022; 93:280.
  134. Moene FC, Spinhoven P, Hoogduin KA, van Dyck R. A randomized controlled clinical trial of a hypnosis-based treatment for patients with conversion disorder, motor type. Int J Clin Exp Hypn 2003; 51:29.
  135. Gelauff J, Stone J, Edwards M, Carson A. The prognosis of functional (psychogenic) motor symptoms: a systematic review. J Neurol Neurosurg Psychiatry 2014; 85:220.
  136. Ibrahim NM, Martino D, van de Warrenburg BP, et al. The prognosis of fixed dystonia: a follow-up study. Parkinsonism Relat Disord 2009; 15:592.
  137. Kim YJ, Pakiam AS, Lang AE. Historical and clinical features of psychogenic tremor: a review of 70 cases. Can J Neurol Sci 1999; 26:190.
  138. Jankovic J, Vuong KD, Thomas M. Psychogenic tremor: long-term outcome. CNS Spectr 2006; 11:501.
  139. Carson A, Stone J, Hibberd C, et al. Disability, distress and unemployment in neurology outpatients with symptoms 'unexplained by organic disease'. J Neurol Neurosurg Psychiatry 2011; 82:810.
  140. Carson AJ, Ringbauer B, Stone J, et al. Do medically unexplained symptoms matter? A prospective cohort study of 300 new referrals to neurology outpatient clinics. J Neurol Neurosurg Psychiatry 2000; 68:207.
Topic 14132 Version 30.0

References

1 : American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 5th ed, American Psychiatric Association, Arlington 2013.

2 : World Health Organization. International Classification of Diseases, 11th Revision (ICD-11). https://www.who.int/classifications/classification-of-diseases (Accessed on October 29, 2021).

3 : Phenomenology and psychopathology related to psychogenic movement disorders.

4 : Psychogenic movement disorders: frequency, clinical profile, and characteristics.

5 : Psychogenic movement disorders in children: a report of 15 cases and a review of the literature.

6 : Clinical Characteristics of Functional Movement Disorders: A Clinic-based Study.

7 : The syndrome of fixed dystonia: an evaluation of 103 patients.

8 : Psychogenic movement disorders in children.

9 : Functional Movement Disorders in Elderly.

10 : Functional movement disorders are not uncommon in the elderly.

11 : A Review and Expert Opinion on the Neuropsychiatric Assessment of Motor Functional Neurological Disorders.

12 : Incidence and 12-month outcome of non-transient childhood conversion disorder in the U.K. and Ireland.

13 : Assessment of Emergency Department and Inpatient Use and Costs in Adult and Pediatric Functional Neurological Disorders.

14 : Clinical Correlates of Functional Motor Disorders: An Italian Multicenter Study.

15 : Transcultural comparison of psychogenic movement disorders.

16 : Transcultural comparison of psychogenic movement disorders.

17 : Psychogenic tremor and related disorders.

18 : Psychogenic tremor: long-term prognosis in patients with electrophysiologically confirmed disease.

19 : Stressful life events and maltreatment in conversion (functional neurological) disorder: systematic review and meta-analysis of case-control studies.

20 : Motor conversion disorder. A prospective 2- to 5-year follow-up study.

21 : Psychiatric outcome in patients with a psychogenic movement disorder: a prospective study.

22 : Psychopathology and psychogenic movement disorders.

23 : Psychogenic movement disorders.

24 : Long-term prognosis of patients with psychogenic movement disorders.

25 : Physical precipitating factors in functional movement disorders.

26 : Characteristics of patients with motor functional neurological disorder in a large UK mental health service: a case-control study.

27 : Personality disorders and somatization in functional and organic movement disorders.

28 : Psychogenic movement disorders.

29 : Functional or psychogenic: what's the better name?

30 : Mistaken diagnosis of psychogenic gait disorder in a man with status cataplecticus ("limp man syndrome").

31 : Functional/psychogenic movement disorders: do we know what they are?

32 : Neurobiology of functional (psychogenic) movement disorders.

33 : A Bayesian account of 'hysteria'.

34 : Loss of sensory attenuation in patients with functional (psychogenic) movement disorders.

35 : The role of alexithymia in the development of functional motor symptoms (conversion disorder).

36 : Functional dystonia and the borderland between neurology and psychiatry: New concepts.

37 : Impaired self-agency in functional movement disorders: A resting-state fMRI study.

38 : Misdirected attentional focus in functional tremor.

39 : Gray matter differences in patients with functional movement disorders.

40 : Gray matter differences in patients with functional movement disorders.

41 : Immediate response to botulinum toxin injections in patients with fixed dystonia.

42 : Psychogenic movement disorders: diagnosis and management.

43 : Diagnostic and pathophysiological aspects of psychogenic tremors.

44 : How Do I Examine Patients With Functional Tremor?

45 : The resolution of the Latah paradox.

46 : The "Whack-a-Mole" Sign in Functional Movement Disorders.

47 : The hyperekplexias and their relationship to the normal startle reflex.

48 : How typical are 'typical' tremor characteristics? Sensitivity and specificity of five tremor phenomena.

49 : Posttraumatic painful torticollis.

50 : Psychogenic dystonia and peripheral trauma.

51 : Comparison of acute- and delayed-onset posttraumatic cervical dystonia.

52 : The causalgia-dystonia syndrome.

53 : Dystonia in complex regional pain syndrome type I.

54 : Syndrome of fixed dystonia in adolescents--short term outcome in 4 cases.

55 : Peripherally induced oromandibular dystonia.

56 : Can peripheral trauma induce dystonia and other movement disorders? Yes!

57 : Can peripheral trauma induce dystonia? No!

58 : Post-traumatic shoulder dystonia in an active duty soldier.

59 : Abnormality of motor cortex excitability in peripherally induced dystonia.

60 : Peripheral trauma induced dystonia or post-traumatic syndrome?

61 : How psychogenic is dystonia? Views from past to present.

62 : Peripheral trauma and movement disorders: a systematic review of reported cases.

63 : Psychogenic facial movement disorders: clinical features and associated conditions.

64 : Are psychogenic non-epileptic seizures just another symptom of conversion disorder?

65 : Gait abnormalities in psychogenic movement disorders.

66 : How to identify psychogenic disorders of stance and gait. A video study in 37 patients.

67 : Paul Blocq and (psychogenic) astasia abasia.

68 : Psychogenic gait disorders.

69 : Hysterical gait disorders: 60 cases.

70 : Human walking and higher-level gait disorders, particularly in the elderly.

71 : Ten myths about functional neurological disorder.

72 : Interobserver agreement and validity of bedside 'positive signs' for functional weakness, sensory and gait disorders in conversion disorder: a pilot study.

73 : Diagnostic performance of the "Huffing and Puffing" sign in psychogenic (functional) movement disorders.

74 : Identifying patterns of psychogenic gait by video-recording.

75 : The "chair test" to aid in the diagnosis of psychogenic gait disorders.

76 : Propriospinal myoclonus: clinical reappraisal and review of literature.

77 : Psychogenic myoclonus.

78 : Psychogenic myoclonus.

79 : Psychogenic parkinsonism: a combination of clinical, electrophysiological, and [(123)I]-FP-CIT SPECT scan explorations improves diagnostic accuracy.

80 : Psychogenic movement disorders.

81 : Psychogenic parkinsonism.

82 : Diagnosis and treatment of psychogenic parkinsonism.

83 : Cohort study on somatoform disorders in Parkinson disease and dementia with Lewy bodies.

84 : Psychogenic parkinsonism.

85 : The role of DAT-SPECT in movement disorders.

86 : A positive diagnosis of functional (psychogenic) tics.

87 : A positive diagnosis of functional (psychogenic) tics.

88 : Rapid Onset Functional Tic-Like Behaviors in Young Females During the COVID-19 Pandemic.

89 : Mind the Difference Between Primary Tics and Functional Tic-like Behaviors.

90 : What Is the Role of a Specialist Assessment Clinic for FND? Lessons From Three National Referral Centers.

91 : Psychogenic paroxysmal movement disorders--clinical features and diagnostic clues.

92 : "Psychogenic" versus "functional" movement disorders? That is the question.

93 : Clinical decision-making in functional and hyperkinetic movement disorders.

94 : Psychogenic movement disorders.

95 : Psychogenic movement disorders: past developments, current status, and future directions.

96 : Systematic review of misdiagnosis of conversion symptoms and "hysteria".

97 : Diagnosing psychogenic movement disorders-which criteria should be used in clinical practice?

98 : The diagnosis of Parkinson's disease.

99 : Identification of psychogenic, dystonic, and other organic tremors by a coherence entrainment test.

100 : Physiology of psychogenic movement disorders.

101 : Two different pathogenetic mechanisms in psychogenic tremor.

102 : Moving toward "laboratory-supported" criteria for psychogenic tremor.

103 : Validation of "laboratory-supported" criteria for functional (psychogenic) tremor.

104 : Time-frequency analysis of tremors.

105 : Voluntary stimulus-sensitive jerks and jumps mimicking myoclonus or pathological startle syndromes.

106 : Electrophysiological aids to the diagnosis of psychogenic jerks, spasms, and tremor.

107 : What is the Bereitschaftspotential?

108 : What is the Bereitschaftspotential?

109 : Treatment of functional neurological disorder: current state, future directions, and a research agenda.

110 : Trick or treat? Showing patients with functional (psychogenic) motor symptoms their physical signs.

111 : Tremor retrainment as therapeutic strategy in psychogenic (functional) tremor.

112 : Physiotherapy for functional motor disorders: a consensus recommendation.

113 : Occupational therapy consensus recommendations for functional neurological disorder.

114 : Management of functional communication, swallowing, cough and related disorders: consensus recommendations for speech and language therapy.

115 : Physiotherapists and patients with functional (psychogenic) motor symptoms: a survey of attitudes and interest.

116 : Functional movement disorders: successful treatment with a physical therapy rehabilitation protocol.

117 : Psychogenic gait disorder: a randomized controlled trial of physical rehabilitation with one-year follow-up.

118 : Outcomes of a 5-day physiotherapy programme for functional (psychogenic) motor disorders.

119 : Randomised feasibility study of physiotherapy for patients with functional motor symptoms.

120 : Integrated Therapy for Functional Movement Disorders: Time for a Change.

121 : Diagnosing functional neurological disorder: seeing the whole picture.

122 : Antidepressant treatment outcomes of psychogenic movement disorder.

123 : Treatment of functional (psychogenic) movement disorders.

124 : Behavioural interventions in the rehabilitation of acute v. chronic non-organic (conversion/factitious) motor disorders.

125 : OnabotulinumtoxinA and cognitive behavioral therapy in functional dystonia: A pilot randomized clinical trial.

126 : Clinical and neural responses to cognitive behavioral therapy for functional tremor.

127 : Single-blind clinical trial of psychotherapy for treatment of psychogenic movement disorders.

128 : Single-blind clinical trial of psychotherapy for treatment of psychogenic movement disorders.

129 : Motor Retraining (MoRe) for Functional Movement Disorders: Outcomes From a 1-Week Multidisciplinary Rehabilitation Program.

130 : Specialist inpatient treatment for severe motor conversion disorder: a retrospective comparative study.

131 : Inpatient treatment of functional motor symptoms: a long-term follow-up study.

132 : Multidisciplinary treatment for functional neurological symptoms: a prospective study.

133 : Neuromodulation for the treatment of functional neurological disorder and somatic symptom disorder: a systematic review.

134 : A randomized controlled clinical trial of a hypnosis-based treatment for patients with conversion disorder, motor type.

135 : The prognosis of functional (psychogenic) motor symptoms: a systematic review.

136 : The prognosis of fixed dystonia: a follow-up study.

137 : Historical and clinical features of psychogenic tremor: a review of 70 cases.

138 : Psychogenic tremor: long-term outcome.

139 : Disability, distress and unemployment in neurology outpatients with symptoms 'unexplained by organic disease'.

140 : Do medically unexplained symptoms matter? A prospective cohort study of 300 new referrals to neurology outpatient clinics.