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INTRODUCTION AND BACKGROUND — Functional movement disorders (FMDs) are clinical syndromes defined by the occurrence of abnormal involuntary movements that are incongruent with a known neurologic cause and are significantly improved on neurological exam with distraction or nonphysiologic maneuvers . This definition replaces the previous one that considered FMDs to be "psychogenic movement disorders" and attributed the occurrence of the abnormal movements to a psychiatric cause . FMDs were first described in the late 19th and early 20th centuries and have been the subject of great interest and puzzlement ever since [3-5]. In addition to "psychogenic," alternative terms for FMDs include "hysterical" or "nonorganic" movement disorders and "medically unexplained" motor symptoms . In modern times, awareness of FMDs has increased in the movement disorder literature. However, the pathogenesis and pathophysiology of FMDs are not fully understood [1,7-9], and debate continues as to whether "functional" or "psychogenic" is the better term for these movement disorders [10-16].
The dangers of FMDs are manifold: excessive, unnecessary, and costly investigations of FMD resulting in reinforcing the sick role, misdiagnosing organic illness as psychogenic , misdiagnosing FMD as organic, and failure to recognize a kernel of organic illness embedded in the symptoms of a FMD . The prevalence, poor prognosis, and intensive healthcare utilization of FMDs present a problem that has been likened to a crisis in neurology . In order to offer the best chance for remission and to use scarce resources wisely, rapid and accurate diagnosis of FMDs is essential.
This topic will review clinical aspects of FMDs, including epidemiology, clinical features, diagnosis, management, and prognosis.
EPIDEMIOLOGY — The precise incidence and prevalence of FMDs are unknown, as population-based studies are unavailable. Estimates of the prevalence of FMD among adults and children with movement disorders vary between 2 to 4 percent [20-25]. Women are affected more often than men. A retrospective chart review of our center in Toronto yielded 206 patients with a diagnosis of FMD out of 7624 records, for a prevalence of 3 percent . Of note, our center receives referral from both primary care physicians and from other academic movement disorders centers. The prevalence of FMD among patients who present with dystonia and fixed, contracted joints may be even higher. As an example, one study of 41 such patients with prospective data reported that criteria for functional dystonia were fulfilled in 15 (37 percent) .
In most reports of adults and children with FMD, functional tremor is the most frequent type of involuntary movement, followed by functional dystonia [20,27-29]. Among our cohort of 206 patients with FMD, the most common functional involuntary movements were tremor (33 percent), dystonia (25 percent), myoclonus (25 percent), gait disorders (11 percent), and parkinsonism (6 percent) . Women comprised 77 percent of the total cohort. Although our population is culturally diverse, a formal study of transcultural differences that compared patients with FMD from the United States and Spain revealed similar frequencies of movement types, gender, anatomic distribution, and disability across ethnic groups .
Risk factors and precipitating events — Based upon limited and inconsistent data, potential risk factors or precipitating events for FMD include previous injury, infection, surgery, higher rates of childhood trauma, a history of sexual abuse, and major stressful life events [22,31-35]. In an uncontrolled retrospective study of 50 patients with FMD, a physical event occurring within three months of the onset of the FMD was reported by 80 percent . The physical events involved an injury in 11, infection in 9, a neurologic disorder (ie, severe migraine, brachial neuritis, Bell's palsy, carpal tunnel syndrome, restless legs syndrome, and pituitary hemorrhage) in 8, pain in 4, a drug reaction in 3, surgery in 3, and vasovagal syncope in 2 subjects. Symptoms fulfilling diagnostic criteria for panic attack during the physical event were present in 36 percent. These findings suggest that FMDs are commonly triggered by physical events, sometimes in association with symptoms of panic.
ETIOLOGY — FMDs require attention to generate the movements, given that distraction leads to decreased movement of the affected body part, while observation or examination leads to increased movement of the affected body part . However, affected individuals lack a sense that the abnormal movements are under voluntary control. While the mechanisms that cause or contribute to FMDs are an area of uncertainty and controversy , an evolving hypothesis is that FMDs result from a combination of predisposing factors including [1,9,36-38]:
●Abnormal self-directed attention
●Abnormal beliefs and expectations
●Abnormal sense of agency (ie, a subjective sense of control) for self-generated movements
●Alexithymia (impaired emotional processing with difficulty identifying and verbalizing internal emotional states)
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 subjective, normal sense of voluntary control . In patients with alexithymia, emotional or autonomic symptoms that occur with a triggering event may be misinterpreted as being caused by a physical illness . FMDs represent the complex interaction of psychological and physical expression.
Underlying psychiatric disorders — Conversion disorder is probably the most common psychiatric diagnosis among patients with a FMD. Coexisting personality disorders may predispose to FMD. Other psychiatric disorders and diagnoses among patients with FMD may include factitious disorder, anxiety disorders, and depression . Malingering, though not a psychiatric disorder, is probably an uncommon cause of FMD. An awareness of these conditions is important for the clinician caring for a patient with suspected FMD.
●Conversion disorder (functional neurologic symptom disorder) is characterized by neurologic symptoms (eg, weakness, abnormal movements, or nonepileptic seizures) that are inconsistent with a neurologic disease, but nevertheless cause distress and/or psychosocial impairment (table 1). While a psychological factor is often associated with conversion disorder, it is not necessary; a psychological factor is not always readily apparent in patients with nonphysiologic neurologic symptoms. There is no age restriction for onset. (See "Conversion disorder in adults: Terminology, diagnosis, and differential diagnosis".)
●The commonly used terms "somatization," "multiple somatizations," or "somatoform disorders" are used to describe a syndrome of physical symptoms that cannot be explained by a known medical disease and are associated with substantial psychosocial impairment. However, the term "somatization" is not used in the Diagnostic and Statistical Manual, Fifth Edition (DSM-5) . For patients with prominent somatic symptoms that cause distress and impair psychosocial functioning, DSM-5 has replaced the category of somatoform disorders with a category called somatic symptom and related disorders. The different terms and diagnoses used to describe somatization can be confusing (table 2), a problem discussed in detail separately. (See "Somatization: Epidemiology, pathogenesis, clinical features, medical evaluation, and diagnosis".)
●While factitious disorder and malingering are both intentionally feigned or deliberately induced, they are distinguished by motivation.
•Factitious disorder (also known as Munchausen syndrome) refers to intentionally feigned or deliberately induced physical or psychological symptoms in order to assume the sick role in the absence of external rewards. That is, the motivation for factitious disorders is attention for illness. (See "Factitious disorder imposed on self (Munchausen syndrome)".)
•Malingering refers to symptoms that are intentionally feigned or deliberately induced in order to obtain external incentives such as avoiding work, gaining compensation, or obtaining more favorable living arrangements. Malingering is not a psychiatric disorder.
●Personality disorders are characterized by personality traits that are inflexible and maladaptive across a wide range of situations, causing significant distress and impairment of social, occupational, and role functioning (table 3). In addition, the thinking, displays of emotion, impulsivity, and interpersonal behavior of the individual deviate markedly from the expectations of the individual's culture. The most common is the histrionic personality disorder, characterized by pervasive and excessive emotionality and attention-seeking behavior. Other predisposing personality disorders include borderline personality or antisocial personality disorders. (See "Personality disorders".)
The burden of psychiatric disease, psychologic factors and stressors among patients with FMD is illustrated by the following observations:
●A case-control study evaluated 55 subjects with functional motor symptoms, a group that included 39 with FMDs, and compared them with a group of 33 subjects with organic movement disorders and 34 healthy controls . The proportion of subjects with alexithymia was significantly higher in the group with functional motor symptoms compared with the organic movement disorders and healthy control groups (35, 9, and 6 percent, respectively).
●In one report of 49 patients with a FMD, conversion disorder, malingering, and factitious disorder were present in 90, 8, and 2 percent, respectively . In addition, major depression, anxiety disorder, and schizophrenia were diagnosed in 33, 16, and 2 percent, respectively.
●In another study of 42 patients with documented or clinically established FMD, the lifetime prevalence rates of conversion disorder, personality disorders, anxiety disorders, and major depression were 95, 45, 62, and 43 percent, respectively . Additional major psychiatric diagnoses included schizoaffective disorder, bipolar disorder, and substance abuse.
●In a case-control study, 64 adult patients with FMD reported significantly higher rates of childhood trauma (mainly emotional abuse and physical neglect), greater fear associated with traumatic events, and a greater number of traumatic episodes compared with 39 healthy controls and 39 patients with an organic movement disorder (focal hand dystonia) . In addition, patients with FMD had significantly higher scores on measures of depression and anxiety than controls and patients with focal hand dystonia. However, there was no significant difference between groups for rates of sexual or physical abuse, and no significant differences on personality scales between the FMD and healthy control groups.
●History of a precipitating event
●Fast progression to maximum symptom severity and disability
●Movement abnormality that is incongruent with organic disease (eg, bizarre, multiple, or difficult to classify)
●Inconsistency over time with variable amplitude, frequency, or distribution of the movement
●Ability to trigger or relieve the movement with unusual or nonphysiologic intervention (eg, trigger points on the body, application of a tuning fork)
●Decreased movement of the affected body part with distraction
●Increased movement of the affected body part during observation or examination
●Entrainment of movement (eg, tremor) to the frequency of repetitive movements (see 'Examination' below)
●Deliberate slowness of movement
●Association with false (or "give-way") weakness, sensory loss, and pain
●Functional disability out of proportion to exam findings
●Unresponsiveness to drugs for organic movement disorders
●Responsiveness to placebo drugs and suggestion
The main FMD syndromes are functional tremor, functional dystonia, functional gait, functional myoclonus, and functional parkinsonism. These are reviewed in the sections below.
Functional tremor — Functional tremor is the most common type of FMD  (see 'Epidemiology' above). Tremor associated with typical neurologic disorders is defined as a rhythmic and oscillatory movement of a body part with a relatively constant frequency (table 5). Functional tremor is typically a complex resting, postural, and action tremor. The only known organic tremor with such physical findings is a cerebellar outflow or midbrain tremor (ie, rubral tremor) . Any body part may be involved with functional tremor, but hand tremor, leg tremor, and whole body tremor are common sites . Remarkably, the fingers are often spared with much of the upper limb tremor occurring at the wrist [28,43].
A characteristic that suggests functional tremor rather than organic tremors is abrupt onset with immediate maximal severity, often precipitated by trivial emotional or physical trauma . In contrast, essential tremor typically starts bilaterally, though one side usually is affected more than the other, and gradually worsens over years to decades (see "Overview of tremor"). With functional tremor, a classic but not universal finding is complete remission or entrainment (ie, a shift of tremor frequency to the speed of contralateral rhythmic movement) with distraction maneuvers such as repetitive tapping tasks with an uninvolved opposite hand or foot. In some patients with functional tremor, restraining the affected limb may precipitate tremor in other previously unaffected body regions. Another sign of a functional tremor is that it can be "chased." That is, when an affected hand is restrained, the tremor may move to the arm, and when the arm is restrained, the tremor may move to the shoulder. Additionally, the affected limb may "fight" with the examiner when it is restrained. This coactivation sign describes the ongoing isometric contraction of antagonistic muscles that may be perceived on examination as increased muscle tone during passive movement .
Electrophysiologic studies may be helpful in documenting the frequency of the functional tremor and distractibility. (See 'Electrodiagnostic testing' below.)
Functional dystonia — Functional dystonia is the second most common type of FMD in most series. (See 'Epidemiology' above.)
True dystonia is defined as a movement disorder characterized by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements, postures, or both. Dystonic movements are typically patterned, twisting, and may be tremulous. Dystonia is often initiated or worsened by voluntary action and associated with overflow muscle activation (see "Classification and evaluation of dystonia"). Functional dystonia may affect any part of the body or be generalized. Features that suggest a functional etiology include inconsistent dystonic movements over time, dystonia presenting as a fixed posture or a paroxysmal disorder (not due to a known paroxysmal movement disorder), the presence of incongruous dystonic movements and postures (eg, facial grimacing with pulling of the mouth to one side), excessive slowness, marked resistance to passive movements, and multiple somatizations [44-46]. While not necessarily pathognomonic, additional features suggesting functional dystonia include fixed foot dystonia in an adult, the presence of other atypical movements or postures such as a bizarre gait (not fitting the gait pattern of other movement disorders, including true dystonia), dystonia occurring when the affected body part is at rest, and pain as a prominent aspect. Muscle atrophy or joint contractures may be present in longstanding functional dystonia due to disuse or prolonged maintenance of the tonic posture. Muscle hypertrophy may be present due to sustained contracture. Since true dystonia historically has been misdiagnosed as functional dystonia, the examiner should be aware of this diagnostic pitfall.
Peripherally induced dystonia — Dystonia that occurs after peripheral trauma has been described in adults and children and is known by a number of terms, including fixed dystonia, traumatic or post-traumatic dystonia, post-traumatic cervical dystonia, post-traumatic painful torticollis, peripherally induced dystonia, causalgia-dystonia syndrome, and complex regional pain syndrome dystonia (formerly known as reflex sympathetic dystrophy) [26,47-53]. In most cases, the precipitating trauma is minor. The inciting injury may involve nerve root, peripheral nerve, or soft tissue. Although the mechanism of peripherally induced dystonia is controversial [54-60], there is little evidence to support an organic basis, while the overlap with features suggestive of FMD is extensive . Thus, many cases are probably functional.
The following observations illustrate these points:
●One of the larger studies described 103 patients with dystonic postures and joint contractures, including 41 who were prospectively assessed . The majority were women (84 percent) and young (mean age of onset 30 years), with a mean disease duration of five years prior to evaluation. A peripheral back or neck injury preceded onset in 63 percent, and a history of somatization disorder was noted in 22 percent. A psychologic stressor or psychiatric disorder was present at onset in 10 percent. Features of complex regional pain syndrome were present in 41 percent. Functional signs on examination (including give-way weakness, nonanatomic sensory changes, and self-inflicted injuries) were present in 33 percent of the entire cohort, and in 46 percent of the prospective group. Diagnostic investigations revealed no consistent abnormalities to explain dystonia, and genetic testing conducted in 25 patients was negative for the DYT1 mutation, the most common positive genetic abnormality in patients with hereditary dystonia. Criteria for clinically definite functional dystonia were fulfilled by 24 percent of the entire cohort and by 36 percent of the prospective group. Prognosis was poor, with rates of complete remission for the entire cohort and the prospective group of 8 and 10 percent, respectively, although follow-up was relatively short (mean 2.9 and 3.9 years, respectively).
●In a retrospective chart review of 16 patients with post-traumatic painful dystonia, all 16 were seeking compensation through the courts . Unlike other forms of FMD, men and women were equally represented. All had a trivial motor vehicle or work-related accident with abrupt onset shortly after the injury and little or no progression after the first week of onset. All 16 patients had prominent pain. The characteristic posture, a fixed head tilt with shoulder elevation, was present in 15 patients. Nondermatomal sensory loss was present in 14. Intravenous amobarbital improved the posture, pain, or both in all 13 patients undergoing the procedure, and marked or complete remission of sensory deficits occurred for 7 of the 13 patients. Formal psychologic evaluation of 11 patients revealed conflict, stress, or both and a tendency to express distress through somatic complaints.
Functional gait — In functional gait disorders, walking is often bizarre and does not conform to any of the usual patterns observed with neurologic gait disorders (see "Neurologic gait disorders of elderly people", section on 'Neurologic causes'). There may be excessive slowness and stiffness, or maintenance of postural control on a narrow base with flailing arms and excessive trunk sway. Astasia-abasia, an inability to stand (astasia) or walk (abasia) in the absence of other neurologic abnormalities, was the term applied by investigators in the mid to late 19th century to describe certain patients with a frankly functional gait [61,62]. Other descriptive terms include gaits that resemble walking on ice, walking a sticky surface, walking through water (bringing to mind excessive slowness), tightrope walking, habitual limping, and bizarre, robotic, knock-kneed, trepidant, anxious, and cautious gaits [46,63].
Features suggestive of a functional gait disorder are illustrated by the following observations:
●In a report that analyzed the clinical manifestations of functional gait disorder in 37 patients, the following six characteristics were identified as supporting the diagnosis :
•Momentary fluctuations of stance and gait, often in response to suggestion
•Excessive slowness or hesitation of locomotion incompatible with neurologic disease
•A "functional" response to the Romberg test, with a build-up of swaying amplitudes after a silent latency, or with improvement by distraction
•Uneconomic postures that waste muscular energy
•"Walking on ice," characterized by small, cautious steps with fixed ankle joints
•Sudden buckling of the knees, usually without falls
●In a retrospective review of 279 patients with various types of FMD, a functional gait disturbance was paired with additional functional movements in 102 patients (37 percent), and a pure functional gait disturbance in 16 patients (5 percent) . Thus, a functional gait was present in a total of 118 patients (42 percent). The most frequent gait patterns among all 118 patients with a functional gait were excessive slowness (19 percent), dystonic gait (18 percent), bizarre gait (12 percent), astasia-abasia (12 percent), and knee buckling (8 percent). For the 16 patients with a pure functional gait disturbance, the most frequent patterns were knee buckling (31 percent), astasia-abasia (19 percent), and bizarre gait (13 percent). Compared with patients who had another FMD and normal gait, those with a functional gait disorder had more frequent excessive slowing of movements on finger to nose testing and finger or foot tapping.
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 . This type of cautious gait is characterized by a shortened stride, a normal to mildly widened base, slow walking speed, en bloc turns, and mild disequilibrium. Other neurologic symptoms and signs are mild or absent. In contrast to an appropriately cautious gait, patients with an incapacitating fear of falling may exhibit another type of cautious gait described as "space phobia" and characterized by timid walking while holding on to furniture and walls . However, other functional features are typically absent . In addition to appropriate caution and fear of falling, the differential diagnosis of cautious gait includes higher level organic gait disorders. (See "Neurologic gait disorders of elderly people", section on 'Frontal lobe dysfunction'.)
Anxiety and depression usually have a minor effect on gait . However, severely depressed patients with psychomotor retardation may walk with reduced stride length and a lifting motion of the legs .
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"). In a report of 212 patients with myoclonus that included 18 patients diagnosed with functional myoclonus, the characteristics of functional myoclonus were as follows :
●Inconsistent character of the movements (amplitude, frequency, and distribution) and other features incongruous with typical "organic" myoclonus
●Associated functional symptomatology
●Marked reduction of the myoclonus with distraction
●Exacerbation and relief with suggestion and placebo
●Spontaneous periods of remission
●Acute onset and sudden resolution
●Evidence of underlying psychopathology
A later systematic review of 179 published cases identified as having propriospinal myoclonus found that the diagnosis was functional myoclonus in 57 percent .
Electrodiagnostic testing can be helpful in differentiating functional myoclonus from true myoclonus. (See 'Electrodiagnostic testing' below.)
Startle syndromes — Startle is a physiologic generalized myoclonic response to an unexpected auditory, visual, somatosensory, or vestibular stimulus that occurs in normal individuals. It consists of a short latency stereotyped blink, facial grimace, or brisk flexion of the neck, trunk, and upper limbs [71,72]. Normal startle is characterized by consistent latency of response after stimulation and rapid habituation to repetitive stimulation. Patients with pathologic exaggerated startle (hyperekplexia) do not habituate. Sporadic and hereditary forms of hyperekplexia are considered organic and can produce generalized myoclonus [72,73]. Patients with functional startle tend to have an exaggerated initial startle response that habituates to repetitive stimulation but shows inconsistent latencies .
Culturally determined forms of startle presumed to be functional in origin include the latah syndrome of Malaysia and Indonesia, the Jumping Frenchmen of Maine, the Ragin' Cajuns of Louisiana, and the miryachit phenomenon of eastern Siberia [75-78]. A psychodynamic explanation of these forms of excessive startle is that they represent an environment-dependent behavior determined by culture, isolation, and familial behavior, particularly in the case of the orienting behaviors. These may include automatic obedience, echopraxia, perseveration of simple movements, vocalizations, and coprolalia .
Functional parkinsonism — The motor manifestations of true parkinsonism are the presence of rest tremor, bradykinesia, rigidity, and postural instability (see "Clinical manifestations of Parkinson disease", section on 'Cardinal manifestations'). The manifestations of functional parkinsonism can be superficially similar but have features suggesting a functional origin (see 'Clinical features' above).
Unlike a parkinsonian 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 [46,79-81]. The tremor will typically increase with attention and decrease with distraction . With functional bradykinesia, movements are slow and effortful, but usually lack the typical reduction in speed or amplitude that is observed with successive movements in true bradykinesia. Increased muscle tone is a result of voluntary opposition rather than the true rigidity (ie, involuntary resistance to passive movement) seen with parkinsonism, and cogwheeling is absent. Atypical gait abnormalities and postural instability are often present, but postural stability testing may reveal bizarre responses such as arm flailing and reeling backward without falling.
Features of functional parkinsonism may coexist with organic Parkinson disease, and some evidence suggests that functional parkinsonism or other somatoform disorders can be an early manifestation of Parkinson disease [82,83].
●In a study of 14 patients with functional parkinsonism, tremor was present in 12, balance and gait difficulties were present in 12, and rigidity with voluntary resistance was noted in 6 . Nonphysiologic weakness and sensory disturbances were present in 10 patients.
●In another report of nine patients referred for suspicion of functional parkinsonism who were followed for at least two years, the final diagnosis was pure functional parkinsonism for four patients and a combination of functional parkinsonism with Parkinson disease for five patients . Common clinical features in this group included the sudden onset of symptoms; precipitation by emotional, physical, financial, or legal factors; marked disability despite short duration of symptoms; false neurologic signs; atypical tremor (violent shaking of one arm, generalized violent shaking, distractibility); gegenhalten tone; lack of response to adequate levodopa treatment trials; and psychological disturbances including depression, anxiety, personality, or bipolar disorder. For one patient who was initially misdiagnosed as having combined functional parkinsonism and Parkinson disease, clinical follow-up and persistently normal single photon emission computed tomography (SPECT) scan findings excluded Parkinson disease and supported the final diagnosis of pure functional parkinsonism.
A normal dopamine transporter imaging study using SPECT scan is helpful for supporting a diagnosis of functional, drug-induced, or vascular parkinsonism by excluding true nigrostriatal degeneration . However, 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 'Neuroimaging' below and "Diagnosis and differential diagnosis of Parkinson disease", section on 'DaTscan'.)
DIAGNOSIS AND DIFFERENTIAL — The diagnosis of a FMD is based upon clinical impression:
●The diagnosis of FMD requires the presence of characteristic clinical features (table 4), particularly symptoms and signs that are inconsistent over time and incongruent with organic movement disorders [2,7]. Thus, the diagnosis depends on positive criteria and is not merely one of exclusion.
●Coexisting psychologic factors and psychiatric disorders are supportive features for the diagnosis of FMD, but their presence is not required .
●FMD can coexist with organic illness.
●There is no gold standard test for confirming the diagnosis of FMD. However, electrodiagnostic studies can provide additional supportive evidence for the diagnosis of functional tremor and functional myoclonus, and dopamine transporter imaging with SPECT scan can support the diagnosis of functional parkinsonism by excluding organic causes of parkinsonism. (See 'Electrodiagnostic testing' below and 'Neuroimaging' below.)
The diagnosis of FMD is best made by clinicians with expertise in movement disorders. An accurate diagnosis depends not only on the ability to recognize the characteristic features of FMDs, but also on a meticulous knowledge of organic movement disorders and their common and rare variants. To illustrate this point, 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)" and "Corticobasal degeneration".)
Among FMDs, functional dystonia is particularly challenging to diagnose because it is typically a persistent, tonic condition that often manifests as a fixed posture . These features contrast with the variability that is typical of most other FMDs. In addition, they preclude assessment of certain clues that support a functional etiology, such as distractibility, entrainment, and increased movement during observation or examination. Nevertheless, the presentation of fixed dystonia itself is highly suggestive of FMD even in the absence of ability to perform other testing to confirm the diagnosis.
As a note of caution, the literature documents a number of examples of mislabeling FMD [17,18,86]. However, a systematic review published in 2005 found that the misdiagnosis rate for patients with various conversion symptoms, including some with abnormal movements, has been approximately 4 percent since the 1970s . While not specific for FMDs, this finding suggests that the misdiagnosis rate for conversion disorder is not unacceptably high compared with other psychiatric and neurologic disorders .
History — FMDs often begin suddenly with maximal disability at onset after a trivial provocation (eg, lifting a moderate weight or following a nonconcussive motor vehicle accident). In contrast, organic movement disorders typically begin gradually and without provocation, except when the underlying cause is an acute illness such as a stroke. With time, the severity and anatomic distribution of the movements and associated disability tend to increase more or less linearly. As an example, the typical history for cervical dystonia is onset with a gradual pulling, perhaps while sitting at the computer. Over time, head turning is evident during other activities, with more extreme postures appearing. Pain is common in organic cervical dystonia but is not the dominant feature of presentation.
Patients with FMDs often have more than one movement disorder, which can be a helpful clue to the diagnosis. Despite severe disability, FMD often has periods of "complete remission," allowing the sufferer to do select activities unimpeded. Significant remission in response to psychotherapy or to treatment without a pathophysiologic rationale is also suspicious for a functional etiology of a movement disorder. Examples include complete remission of parkinsonian symptoms with herbal remedies , 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 . Similarly, lack of response to appropriate treatment, such as levodopa for Parkinson disease, also increases suspicion for FMD in the proper clinical context . However, this is a nonspecific finding that could also support a diagnosis of atypical parkinsonism.
Social history may provide important clues to FMD. Familiarity with organic illness among family members, acquaintances, or due to employment as a healthcare professional, may predispose to the development of FMD. A history of sexual or physical abuse may be suppressed by patients with FMD and should be considered carefully when interviewing the patient . Collateral history from family members, other clinicians, and healthcare providers is important, especially in obtaining deeply private information such as a history of sexual and physical abuse during childhood.
Examination — Accompanying signs or symptoms are helpful in diagnosing FMD. Nonanatomic sensory change, give-way weakness, and bizarre gaits (eg, walking on a tightrope, histrionic lurching without losing balance) are common in FMD . Patients may have nonphysiologic triggers or relieving factors (eg, tapping the patellar tendon thereby inducing distant myoclonus, or squeezing the neck and inducing forceful neck flexion). Distraction and entrainment are additional characteristics of FMDs, as described in the sections that follow.
Distraction — One of the most important physical findings that can help differentiate FMD from organic movement disorders is distractibility, not to be confused with a sensory trick that allows near or complete normal posture in dystonia. Distracting maneuvers typically diminish the intensity of the movement in FMD. In contrast, distracting maneuvers usually increase intensity of the movement in organic movement disorders. Variation in frequency and amplitude of the movement, especially with tremor, is an additional clue that the movement is functional.
Entrainment — Entrainment is another feature associated with functional tremor. Entrainment is tested by having the patient make voluntary movements at a given frequency with the extremity contralateral to the side under assessment. The psychogenic movement will assume the frequency of the contralateral voluntary movement if entrainment is positive. In particular, functional tremor will entrain (take on the frequency of the unaffected limb during the distracting maneuver) with distraction, while organic tremor typically will increase in amplitude and become more evident with distraction, maintaining the original frequency. However, distracting maneuvers may not be effective in longstanding FMD .
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.
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 [33,43,92-95]. 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 . Changes in frequency are simultaneous when they occur. In contrast, most organic 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 .
Entrainment is a property whereby a tremor synchronizes with the frequency of voluntary tapping of another body part, most often the opposite hand (see 'Entrainment' above). The degree of similarity of tremor frequency with voluntary tapping can be assessed by coherence analysis. Lack of entrainment suggests an organic 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. In longstanding FMD, distracting maneuvers may not be effective, a feature that limits the utility of testing with electrodiagnostic methods such as an accelerometer .
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 [98,99]. 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 .
There are no definitive electrodiagnostic tests for distinguishing functional dystonia from organic dystonia .
Neuroimaging — A normal dopamine transporter imaging study using SPECT scan is helpful for supporting a diagnosis of functional, drug-induced, or vascular parkinsonism . However, 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'.)
Neuroimaging with CT and MRI scans has little utility for the diagnosis of patients with suspected FMD, except to exclude the possibility of an underlying structural abnormality that potentially contradicts the diagnosis of a FMD. However, the diagnosis of FMD depends on positive criteria (table 4) and is not merely one of exclusion.
Classification of diagnostic certainty — Although rather outdated, criteria for degrees of certainty in the diagnosis of a psychogenic movement disorder were first proposed in 1988 and are well known among specialists in this field :
●Documented psychogenic movement disorder – Consistently and persistently relieved by psychotherapy with or without psychotropic medication, or symptoms may be seen to spontaneously remit when the patient is unaware of being observed, as seen in malingering or factitious disorder. (Note that organic movement disorders may demonstrate transient improvement with psychotropic drugs).
●Clinically established psychogenic movement disorder – Inconsistent symptoms and signs, presentation incongruent with the typical presentation of an organic movement disorder, and presence of other functional signs such as false weakness or sensory loss, multiple somatizations, and obvious psychiatric diagnosis.
●Probable psychogenic movement disorder – Inconsistent or incongruent with an organic movement disorder but lacking other features listed above, abnormal movements that are consistent and congruent with an organic disorder and coexistent functional signs such as false weakness or sensory loss, or movements consistent and congruent with an organic disorder but manifest multiple somatizations.
●Possible psychogenic movement disorder – Movements consistent and congruent with an organic disorder, but other features are present that raise the level of suspicion that the diagnosis is functional in nature. These features include inappropriate affect, a discrepancy between the movement disorder, and the reported disability or the presence of secondary gain.
A few subsequent reports have attempted to validate and revise these original criteria [2,22,101], but the clinical value of the original and revised versions is uncertain , particularly as the field has moved away from the notion that FMDs are inextricably tied to an underlying psychiatric diagnosis. Even so, some data suggest that most patients with FMD have a conversion disorder (see 'Underlying psychiatric disorders' above). Therefore, it is important to look carefully for a treatable underlying psychiatric disorder such as depression or anxiety.
MANAGEMENT — Optimal management of FMDs consists of early diagnosis, providing the patient a credible explanation of the diagnosis, curtailing investigations, and a multidisciplinary approach to treatment.
Explaining the diagnosis — Informing the patient of the diagnosis of FMD is often problematic, especially if the term "psychogenic" is used; most patients do not accept that the trouble may be psychiatric, and many become alienated and seek another opinion . It is the role of the neurologist to make and convey the diagnosis of FMD because most psychiatrists lack sufficient expertise in movement disorders. While some experts still use the term "psychogenic" when telling the patient of the diagnosis of FMD [12,14,16], we and other experts believe that the term "functional" movement disorder is preferred because it is more acceptable to the patient, and because many patients with FMDs have no obvious psychopathology [1,11,13,15]. "Functional" implies that the structure of the nervous system is intact but the function is disordered. In our clinical experience, treatment includes disclosing the diagnosis to the patient with emphasis that the problem is not "made up" by the patient or "in their head."
Except for rare patients with a factitious disorder or malingering, it is important to take the patient's complaints seriously, let the patient know that the condition is "real" and involuntary, and that it is a relatively common disorder. It is also important to tell the patient that the main components of the neurologic examination are normal, and that there is potential for recovery [19,46,102]. Some neurologists find it useful to review symptoms with the patient using a website, www.neurosymptoms.org, which presents balanced information about functional neurologic disorders. Showing the patient their neurologic signs may be a valuable way to help the patient accept the diagnosis .
It is also advisable to tell the patient that the best approach to treatment is multidisciplinary, with referral to a movement disorders center with expertise in treating FMDs.
Treatment options — A multidisciplinary treatment regimen emphasizing physical therapy and aimed at restoring movement and function is the preferred approach for the management of most patients with FMDs . However, there are no proven or universally accepted treatments for FMDs. The evidence supporting available treatments mainly comes from small retrospective studies, and large, randomized controlled trials are lacking. Treatments that may be helpful include physical therapy and occupational therapy [102,104-106], psychotherapy with or without pharmacotherapy , cognitive behavioral therapy [105,108], antidepressant medications , mild to moderate exercise , transcranial magnetic stimulation [105,111,112], and hypnosis [105,113]. For patients with functional tremor, preliminary data suggest that the clinical feature of entrainment (see 'Entrainment' above) can be used as a therapeutic strategy to retrain the tremor frequency and reduce the tremor severity .
Psychiatric interventions are individualized according to the underlying psychiatric diagnosis, and are best accomplished by involvement with a psychiatrist or psychologist who is familiar with FMDs, usually accessible by referral to an established movement disorders center. (See 'Underlying psychiatric disorders' above.)
Evidence supporting an intensive outpatient rehabilitation program protocol comes from a retrospective unblinded study of 60 consecutive patients with a chronic FMD (median duration 18 months) who were treated with a structured motor-reprogramming treatment protocol involving physical and occupational therapy twice daily for five consecutive days . The goal was to restore normal movement patterns. Therapy sometimes involved distracting motor tasks to extinguish abnormal movements. Patients were evaluated by a psychiatrist or psychologist to identify possible causes or contributory factors, but the emphasis was on relearning normal motor patterns rather than on uncovering psychological factors that may have preceded the FMD. The following observations were made :
●At one week, the proportion of the intervention group that was markedly improved, nearly normal, or in remission by physician assessment was 73 percent.
●For long-term outcome, 48 subjects in treatment group (median 25 months of follow-up) could be contacted by questionnaire or phone; the proportion markedly improved, nearly normal, or in remission was 60 percent, compared with 22 percent in a control group of 32 patients with FMD (median 33 months of follow-up) who had usual treatment and were available by questionnaire or phone contact.
●In both groups, most patients (approximately 88 percent) continued to have some degree of abnormal movements.
Further prospective studies are needed to confirm whether this approach is truly effective. A major drawback is that the availability of specialists to implement this motor reprogramming protocol is limited.
Multidisciplinary inpatient treatment of FMD lasting weeks to months has been employed by a few specialized centers in Canada and the United Kingdom, with one study of 32 patients reporting resolution of symptoms in 81 percent . In an observational study that prospectively followed 42 patients with fixed dystonia, most of whom fulfilled criteria for FMD at the level of "probable" or higher, lasting improvement was seen for all 7 patients who received multidisciplinary inpatient treatment combining psychotherapy, cognitive behavioral therapy, physiotherapy, and occupational therapy . These uncontrolled data suggest but do not prove that a multidisciplinary inpatient treatment approach is effective for FMD. However, inpatient treatment for FMD is generally not a viable option in the United States due to insurance restrictions.
Given the available data and our clinical experience, we suggest multidisciplinary treatment in a rehabilitation facility combining physical therapy, occupational therapy, cognitive behavioral therapy, and psychotherapy for patients with FMD rather than outpatient treatment. We suggest multidisciplinary outpatient treatment using the same modalities when inpatient treatment is not an option, usually because of lack of insurance coverage.
As part of the multidisciplinary management of FMDs, other approaches can be considered. Spiritual counselling may be helpful for some individuals. The opportunity to "save face" is important for patients. Clinicians must be inventive to give patients an "out" from their FMD. Some patients have responded to light physical pressure or touch, suggestion, prayer, and other nonconventional interventions. As an example, applying minimal finger pressure on the patient's chest, along with the suggestion that this maneuver will make the movement stop, has been successful on occasion.
PROGNOSIS — Prognosis for complete remission with longstanding FMD is generally poor [19,31,116]. In one prospective study of 42 subjects with FMD who were followed for a mean of three years, abnormal movements persisted in 90 percent . In a retrospective study with self-reported outcome data for 122 patients with FMD who had a mean duration of symptoms of 4.7 years and a mean follow-up of 3.4 years, there was improvement, no change, or worsening in 57, 21, and 22 percent, respectively .
Although data are limited, the following factors have been associated with a poor prognosis for FMD [31,34,117]:
●Long duration of illness
●Insidious onset of symptoms
●Inconsistency of movements
●Dissatisfaction with physician
Factors associated with a more favorable FMD prognosis include the following [31,34,117]:
●Short duration of symptoms (<1 year)
●High patient satisfaction with care
●Good physical health
●Positive social life perception
●Elimination of stressors
There is conflicting evidence regarding the correlation of prognosis with pending litigation, age, comorbid anxiety and depression, intelligence quotient, educational status, and marital status .
SUMMARY AND RECOMMENDATIONS
●Functional (psychogenic) movement disorders (FMDs) are clinical syndromes defined by the occurrence of movements that are incongruent with movement disorders known to be caused by neurologic disease and by significant improvement with distraction or nonphysiologic maneuvers. (See 'Introduction and background' above.)
●Prevalence estimates among adults and children suggest that FMDs account for 2 to 4 percent of all movement disorders. Functional tremor is the most frequent type of involuntary movement with FMD, followed by functional dystonia. (See 'Epidemiology' above.)
●One hypothesis is that FMDs result from a combination of abnormal self-directed attention, abnormal beliefs and expectations, an abnormal sense of agency for self-generated movements, and alexithymia (impaired emotional processing with difficulty identifying and verbalizing internal emotional states). 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 subjective, normal sense of voluntary control. (See 'Etiology' above.)
●A number of clinical characteristics (table 4) are associated with FMDs. The main FMD syndromes are functional tremor, functional dystonia, functional gait, functional myoclonus, and functional parkinsonism.
•Functional tremor is typically a complex resting, postural, and action tremor of abrupt onset. Any body part may be involved although the fingers are often spared. (See 'Functional tremor' above.)
•Functional dystonia may affect any part of the body or be generalized. Features include inconsistent dystonic movements over time, dystonia presenting as a fixed posture or a paroxysmal disorder, the presence of incongruous dystonic movements and postures, excessive slowness, marked resistance to passive movements, multiple somatizations, foot dystonia in an adult, and pain as a prominent aspect. (See 'Functional dystonia' above.)
•Dystonia that occurs after peripheral trauma is known by a number of terms, including fixed dystonia, traumatic or post-traumatic dystonia, post-traumatic cervical dystonia, post-traumatic painful torticollis, peripherally induced dystonia, causalgia-dystonia syndrome, and complex regional pain syndrome dystonia. Although controversial, many cases are probably functional. (See 'Peripherally induced dystonia' above.)
•In functional gait disorders, walking is often bizarre and does not conform to any of the usual patterns observed with neurologic gait disorders. (See 'Functional gait' above.)
•The characteristics of functional myoclonus include features similar to other FMDs such as acute onset, spontaneous periods of remission, inconsistent character of the movements in terms of amplitude, frequency, and distribution, and marked reduction with distraction. (See 'Functional myoclonus' above.)
•The tremor of functional parkinsonism shares the characteristics of isolated functional tremor, manifesting as a complex resting, postural, and action tremor with abrupt onset, a static course, and changeable features. With functional bradykinesia, movements are slow and effortful, but usually lack the typical reduction in speed or amplitude that is observed with successive movements in true bradykinesia. Increased muscle tone is a result of voluntary opposition rather than true rigidity seen with parkinsonism, and cogwheeling is absent. Atypical gait abnormalities and postural instability are often present, but postural stability testing may reveal bizarre responses. (See 'Functional parkinsonism' above.)
●The diagnosis of FMD requires the presence of characteristic clinical features, particularly symptoms and signs that are inconsistent over time and incongruent with organic movement disorders, and decreased movement with distraction (table 4). Thus, the diagnosis depends on positive criteria and is not merely one of exclusion. Coexisting psychologic factors and psychiatric disorders are supportive features for the diagnosis, but their presence is not required. Electrodiagnostic studies can provide additional supportive evidence for the diagnosis of functional tremor and functional myoclonus, and dopamine transporter imaging with single photon emission computed tomography (SPECT) scan can support the diagnosis of functional parkinsonism by excluding organic causes of parkinsonism. (See 'Diagnosis and differential' above.)
●Optimal management of FMDs consists of early diagnosis, providing the patient a credible explanation of the diagnosis, and a multidisciplinary treatment regimen emphasizing physical therapy and aimed at restoring movement and function. However, there is no proven or universally accepted treatment for FMDs. (See 'Management' above.)
●Prognosis for complete remission with longstanding FMD is generally poor. However, factors associated with a more favorable prognosis include short duration of symptoms, early diagnosis, and high patient satisfaction with care. (See 'Prognosis' above.)
- Edwards MJ, Fotopoulou A, Pareés I. Neurobiology of functional (psychogenic) movement disorders. Curr Opin Neurol 2013; 26:442.
- Gupta A, Lang AE. Psychogenic movement disorders. Curr Opin Neurol 2009; 22:430.
- Charcot JM. Hystero-epilepsy: A young woman with a convulsive attack in the auditorium. In: Charcot, the clinician: The Tuesday lessons: Excerpts from nine case presentations on general neurology delivered at the Salpêtrière hospital in 1887–88, Goetz CG (Ed), Raven Press, New York 1987. p.102.
- Gowers WR. A Manual of Diseases of the Nervous System, P Blakiston Son & Co, Philadelphia 1886.
- Head H. An Address ON THE DIAGNOSIS OF HYSTERIA. Br Med J 1922; 1:827.
- Thenganatt MA, Jankovic J. Psychogenic movement disorders. Neurol Clin 2015; 33:205.
- Lang AE, Voon V. Psychogenic movement disorders: past developments, current status, and future directions. Mov Disord 2011; 26:1175.
- Carson AJ, Brown R, David AS, et al. Functional (conversion) neurological symptoms: research since the millennium. J Neurol Neurosurg Psychiatry 2012; 83:842.
- Edwards MJ, Adams RA, Brown H, et al. A Bayesian account of 'hysteria'. Brain 2012; 135:3495.
- Edwards MJ, Stone J, Lang AE. Functional/psychogenic movement disorders: do we know what they are? Mov Disord 2014; 29:1696.
- Edwards MJ, Stone J, Lang AE. From psychogenic movement disorder to functional movement disorder: it's time to change the name. Mov Disord 2014; 29:849.
- Fahn S, Olanow CW. "Psychogenic movement disorders": they are what they are. Mov Disord 2014; 29:853.
- Ganos C, Erro R, Bhatia KP, Tinazzi M. Comment on psychogenic versus functional movement disorders. Mov Disord 2014; 29:1696.
- Jankovic J. "Psychogenic" versus "functional" movement disorders? That is the question. Mov Disord 2014; 29:1697.
- LaFaver K, Hallett M. Functional or psychogenic: what's the better name? Mov Disord 2014; 29:1698.
- Fahn S, Olanow CW. Reply to: psychogenic movement disorders: what's in a name? Mov Disord 2014; 29:1699.
- 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.
- Bentivoglio AR, Loi M, Valente EM, et al. Phenotypic variability of DYT1-PTD: does the clinical spectrum include psychogenic dystonia? Mov Disord 2002; 17:1058.
- Hallett M. Psychogenic movement disorders: a crisis for neurology. Curr Neurol Neurosci Rep 2006; 6:269.
- Miyasaki J. Unpublished data, Morton and Gloria Shulman Movement Disorders Centre, Toronto Western Hospital, Univeristy of Toronto.
- Ertan S, Uluduz D, Ozekmekçi S, et al. Clinical characteristics of 49 patients with psychogenic movement disorders in a tertiary clinic in Turkey. Mov Disord 2009; 24:759.
- Williams DT, Ford B, Fahn S. Phenomenology and psychopathology related to psychogenic movement disorders. Adv Neurol 1995; 65:231.
- Factor SA, Podskalny GD, Molho ES. Psychogenic movement disorders: frequency, clinical profile, and characteristics. J Neurol Neurosurg Psychiatry 1995; 59:406.
- Portera-Cailliau C, Victor D, Frucht S, Fahn S. Movement disorders fellowship training program at Columbia University Medical Center in 2001-2002. Mov Disord 2006; 21:479.
- 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.
- Schrag A, Trimble M, Quinn N, Bhatia K. The syndrome of fixed dystonia: an evaluation of 103 patients. Brain 2004; 127:2360.
- Kirsch DB, Mink JW. Psychogenic movement disorders in children. Pediatr Neurol 2004; 30:1.
- Bhatia KP, Schneider SA. Psychogenic tremor and related disorders. J Neurol 2007; 254:569.
- McKeon A, Ahlskog JE, Bower JH, et al. Psychogenic tremor: long-term prognosis in patients with electrophysiologically confirmed disease. Mov Disord 2009; 24:72.
- Cubo E, Hinson VK, Goetz CG, et al. Transcultural comparison of psychogenic movement disorders. Mov Disord 2005; 20:1343.
- 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.
- Kranick S, Ekanayake V, Martinez V, et al. Psychopathology and psychogenic movement disorders. Mov Disord 2011; 26:1844.
- Hinson VK, Haren WB. Psychogenic movement disorders. Lancet Neurol 2006; 5:695.
- Thomas M, Vuong KD, Jankovic J. Long-term prognosis of patients with psychogenic movement disorders. Parkinsonism Relat Disord 2006; 12:382.
- Pareés I, Kojovic M, Pires C, et al. Physical precipitating factors in functional movement disorders. J Neurol Sci 2014; 338:174.
- Pareés I, Brown H, Nuruki A, et al. Loss of sensory attenuation in patients with functional (psychogenic) movement disorders. Brain 2014; 137:2916.
- 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.
- Newby R, Alty J, Kempster P. Functional dystonia and the borderland between neurology and psychiatry: New concepts. Mov Disord 2016; 31:1777.
- American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), American Psychiatric Association, Arlington 2013.
- 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.
- Gajos A, Bogucki A, Schinwelski M, et al. The clinical and neuroimaging studies in Holmes tremor. Acta Neurol Scand 2010; 122:360.
- Thomas M, Jankovic J. Psychogenic movement disorders: diagnosis and management. CNS Drugs 2004; 18:437.
- Deuschl G, Köster B, Lücking CH, Scheidt C. Diagnostic and pathophysiological aspects of psychogenic tremors. Mov Disord 1998; 13:294.
- Fahn S, Williams DT. Psychogenic dystonia. Adv Neurol 1988; 50:431.
- Lang AE. Psychogenic dystonia: a review of 18 cases. Can J Neurol Sci 1995; 22:136.
- Peckham EL, Hallett M. Psychogenic movement disorders. Neurol Clin 2009; 27:801.
- Sa DS, Mailis-Gagnon A, Nicholson K, Lang AE. Posttraumatic painful torticollis. Mov Disord 2003; 18:1482.
- Hawley JS, Weiner WJ. Psychogenic dystonia and peripheral trauma. Neurology 2011; 77:496.
- Tarsy D. Comparison of acute- and delayed-onset posttraumatic cervical dystonia. Mov Disord 1998; 13:481.
- Bhatia KP, Bhatt MH, Marsden CD. The causalgia-dystonia syndrome. Brain 1993; 116 ( Pt 4):843.
- Lang AE, Chen R. Dystonia in complex regional pain syndrome type I. Ann Neurol 2010; 67:412.
- 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.
- Sankhla C, Lai EC, Jankovic J. Peripherally induced oromandibular dystonia. J Neurol Neurosurg Psychiatry 1998; 65:722.
- Jankovic J. Can peripheral trauma induce dystonia and other movement disorders? Yes! Mov Disord 2001; 16:7.
- Weiner WJ. Can peripheral trauma induce dystonia? No! Mov Disord 2001; 16:13.
- Carroll CG, Hawley JS, Ney JP. Post-traumatic shoulder dystonia in an active duty soldier. Mil Med 2006; 171:494.
- Bohlhalter S, Leon-Sarmiento FE, Hallett M. Abnormality of motor cortex excitability in peripherally induced dystonia. Mov Disord 2007; 22:1186.
- Kumar H, Jog M. Peripheral trauma induced dystonia or post-traumatic syndrome? Can J Neurol Sci 2011; 38:22.
- Munts AG, Koehler PJ. How psychogenic is dystonia? Views from past to present. Brain 2010; 133:1552.
- 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.
- Okun MS, Koehler PJ. Paul Blocq and (psychogenic) astasia abasia. Mov Disord 2007; 22:1373.
- Sudarsky L. Psychogenic gait disorders. Semin Neurol 2006; 26:351.
- Keane JR. Hysterical gait disorders: 60 cases. Neurology 1989; 39:586.
- 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.
- Baik JS, Lang AE. Gait abnormalities in psychogenic movement disorders. Mov Disord 2007; 22:395.
- Nutt JG, Marsden CD, Thompson PD. Human walking and higher-level gait disorders, particularly in the elderly. Neurology 1993; 43:268.
- Marks I. Space "phobia": a pseudo-agoraphobic syndrome. J Neurol Neurosurg Psychiatry 1981; 44:387.
- Sloman L, Berridge M, Homatidis S, et al. Gait patterns of depressed patients and normal subjects. Am J Psychiatry 1982; 139:94.
- Monday K, Jankovic J. Psychogenic myoclonus. Neurology 1993; 43:349.
- van der Salm SM, Erro R, Cordivari C, et al. Propriospinal myoclonus: clinical reappraisal and review of literature. Neurology 2014; 83:1862.
- Brown P, Rothwell JC, Thompson PD, et al. The hyperekplexias and their relationship to the normal startle reflex. Brain 1991; 114 ( Pt 4):1903.
- Bhidayasiri R, Truong DD. Startle syndromes. Handb Clin Neurol 2011; 100:421.
- Harvey RJ, Topf M, Harvey K, Rees MI. The genetics of hyperekplexia: more than startle! Trends Genet 2008; 24:439.
- 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.
- Simons RC. The resolution of the Latah paradox. J Nerv Ment Dis 1980; 168:195.
- Saint-Hilaire MH, Saint-Hilaire JM, Granger L. Jumping Frenchmen of Maine. Neurology 1986; 36:1269.
- McFarling DA. The "Ragin' Cajuns" of Louisiana. Mov Disord 2001; 16:531.
- Bakker MJ, van Dijk JG, Pramono A, et al. Latah: an Indonesian startle syndrome. Mov Disord 2013; 28:370.
- Miyasaki JM, Sa DS, Galvez-Jimenez N, Lang AE. Psychogenic movement disorders. Can J Neurol Sci 2003; 30 Suppl 1:S94.
- Lang AE, Koller WC, Fahn S. Psychogenic parkinsonism. Arch Neurol 1995; 52:802.
- Jankovic J. Diagnosis and treatment of psychogenic parkinsonism. J Neurol Neurosurg Psychiatry 2011; 82:1300.
- 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.
- Hallett M. Psychogenic parkinsonism. J Neurol Sci 2011; 310:163.
- 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.
- Kägi G, Bhatia KP, Tolosa E. The role of DAT-SPECT in movement disorders. J Neurol Neurosurg Psychiatry 2010; 81:5.
- Ranawaya R, Riley D, Lang A. Psychogenic dyskinesias in patients with organic movement disorders. Mov Disord 1990; 5:127.
- Stone J, Smyth R, Carson A, et al. Systematic review of misdiagnosis of conversion symptoms and "hysteria". BMJ 2005; 331:989.
- 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.
- Suchowersky O. Personal communication. 2006.
- Edwards MJ, Bhatia KP, Cordivari C. Immediate response to botulinum toxin injections in patients with fixed dystonia. Mov Disord 2011; 26:917.
- Glosser DS, Stern MB. Psychogenic movement disorders: Theoretical and clinical considerations. In: Parkinson's Disease and Movement Disorders: Diagnosis and Treatment Guidelines for the Practicing Physician, Adler CH, Ahlskog JE (Eds), Humana Press, Totowa, NJ 2000. p.435.
- McAuley J, Rothwell J. Identification of psychogenic, dystonic, and other organic tremors by a coherence entrainment test. Mov Disord 2004; 19:253.
- Raethjen J, Kopper F, Govindan RB, et al. Two different pathogenetic mechanisms in psychogenic tremor. Neurology 2004; 63:812.
- Schwingenschuh P, Katschnig P, Seiler S, et al. Moving toward "laboratory-supported" criteria for psychogenic tremor. Mov Disord 2011; 26:2509.
- Schwingenschuh P, Saifee TA, Katschnig-Winter P, et al. Validation of "laboratory-supported" criteria for functional (psychogenic) tremor. Mov Disord 2016; 31:555.
- O'Suilleabhain PE, Matsumoto JY. Time-frequency analysis of tremors. Brain 1998; 121 ( Pt 11):2127.
- Hallett M. Physiology of psychogenic movement disorders. J Clin Neurosci 2010; 17:959.
- 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.
- Brown P, Thompson PD. Electrophysiological aids to the diagnosis of psychogenic jerks, spasms, and tremor. Mov Disord 2001; 16:595.
- Shibasaki H, Hallett M. What is the Bereitschaftspotential? Clin Neurophysiol 2006; 117:2341.
- Shill H, Gerber P. Evaluation of clinical diagnostic criteria for psychogenic movement disorders. Mov Disord 2006; 21:1163.
- 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.
- Stone J, Edwards M. Trick or treat? Showing patients with functional (psychogenic) motor symptoms their physical signs. Neurology 2012; 79:282.
- Nielsen G, Stone J, Matthews A, et al. Physiotherapy for functional motor disorders: a consensus recommendation. J Neurol Neurosurg Psychiatry 2015; 86:1113.
- Ricciardi L, Edwards MJ. Treatment of functional (psychogenic) movement disorders. Neurotherapeutics 2014; 11:201.
- Nielsen G, Stone J, Edwards MJ. Physiotherapy for functional (psychogenic) motor symptoms: a systematic review. J Psychosom Res 2013; 75:93.
- 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.
- 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.
- Voon V, Lang AE. Antidepressant treatment outcomes of psychogenic movement disorder. J Clin Psychiatry 2005; 66:1529.
- Dallocchio C, Arbasino C, Klersy C, Marchioni E. The effects of physical activity on psychogenic movement disorders. Mov Disord 2010; 25:421.
- Dafotakis M, Ameli M, Vitinius F, et al. [Transcranial magnetic stimulation for psychogenic tremor - a pilot study]. Fortschr Neurol Psychiatr 2011; 79:226.
- Garcin B, Roze E, Mesrati F, et al. Transcranial magnetic stimulation as an efficient treatment for psychogenic movement disorders. J Neurol Neurosurg Psychiatry 2013; 84:1043.
- 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.
- Espay AJ, Edwards MJ, Oggioni GD, et al. Tremor retrainment as therapeutic strategy in psychogenic (functional) tremor. Parkinsonism Relat Disord 2014; 20:647.
- 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.
- Crimlisk HL, Bhatia K, Cope H, et al. Slater revisited: 6 year follow up study of patients with medically unexplained motor symptoms. BMJ 1998; 316:582.
- 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.