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Official reprint from UpToDate

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2013 UpToDate

Psychogenic movement disorders

Author
Janis M Miyasaki, MD, MEd

Section Editor
Howard I Hurtig, MD

Deputy Editor
John F Dashe, MD, PhD

Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Dec 2012. | This topic last updated: Jan 16, 2013.
INTRODUCTION AND BACKGROUND Psychogenic movement disorder (PMD) is a clinical syndrome
defined as the occurrence of abnormal movements that result from a psychiatric cause rather than a general
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medical or neurologic cause [1]. Psychogenic movement disorders were first described in the late 19 and early
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20 centuries and have been the subject of great interest and puzzlement ever since [2-4]. Alternative terms for
PMD include hysterical movement disorder, functional movement disorder, nonorganic movement disorder, and
medically unexplained motor symptoms [5]. In modern times, awareness of PMDs has increased in the
movement disorder literature. However, the pathogenesis and pathophysiology of PMDs remain poorly
understood [6-8].
The dangers of PMDs are manifold: excessive investigation of PMD resulting in reinforcing the sick roll,
misdiagnosing organic illness as psychogenic [9], misdiagnosing PMD as organic, and failure to recognize a
kernel of organic illness embedded in the symptoms of a PMD [10]. The prevalence, poor prognosis, and
intensive healthcare utilization of PMDs present a problem that has been likened to a crisis in neurology [11]. In
order to offer the best chance for remission and to use scarce resources wisely, rapid and accurate diagnosis of
psychogenic movement disorders is essential.
This topic will review clinical aspects of PMDs, including epidemiology, clinical features, diagnosis, management
and prognosis.
EPIDEMIOLOGY The precise incidence and prevalence of PMD are unknown, as population-based studies
are unavailable. Estimates of the prevalence of PMD among adults and children with movement disorders vary
between 2 to 4 percent [12-17]. Women are affected more often than men. A retrospective chart review of our
center in Toronto yielded 206 patients with a diagnosis of PMD out of 7624 records, for a prevalence of 3 percent
[12]. Of note, our center receives referral from both primary care physicians and from other academic movement
disorders centers. The prevalence of PMD 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
psychogenic dystonia were fulfilled in 15 (37 percent) [18].
In most reports of adults and children with PMD, psychogenic tremor is the most frequent type of involuntary
movement, followed by psychogenic dystonia [12,19-21]. Among our cohort of 206 patients with PMD, the most
common psychogenic involuntary movements were tremor (33 percent), dystonia (25 percent), myoclonus (25
percent), gait disorders (11 percent), and parkinsonism (6 percent) [12]. Women comprised 77 percent of the
total cohort. Although our population is culturally diverse, a formal study of transcultural differences that
compared patients with PMD from the United States and Spain revealed similar frequencies of movement types,
gender, anatomic distribution, and disability across ethnic groups [22].
Risk factors Based upon limited and inconsistent data, potential risk factors for PMD include a history of
sexual abuse, previous surgery or other physical trauma, higher rates of childhood trauma, and major stressful
life events [14,23-26].
UNDERLYING PSYCHIATRIC DISORDERS Conversion disorder is probably the most common mechanism
of PMD, and coexisting personality disorders may predispose to PMD. Other psychiatric disorders and
diagnoses among patients with PMD may include somatization, factitious disorder, anxiety disorders, and

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depression [27]. Malingering, though not a psychiatric disorder, is probably an uncommon cause of PMD. An
awareness of these conditions is important for the clinician caring for a patient with suspected PMD.
Conversion disorder is characterized by neurologic symptoms involving motor or sensory function that are
not explained by a neurologic or medical disease, are not intentionally produced or feigned, and are
temporally associated with psychologic factors such as conflict or other stressors (table 1). While a
psychological factor is often associated with conversion disorder, there is growing awareness that it is not
necessary; a psychological factor is not always readily apparent in patients with non-physiological
neurologic symptoms. There is no age restriction for onset.
The 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. In one system (DSM-IV-TR), conversion disorder is considered
a subtype of somatoform disorder (table 2). The different terms and diagnoses used to describe
somatization can be confusing, 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 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 and 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 attentionseeking 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 PMD is illustrated by
the following observations:
In one report of 49 patients with a PMD, conversion disorder, malingering, and factitious disorder were
present in 90, 8 and 2 percent, respectively [13]. 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 PMD, the lifetime prevalence
rates of conversion disorder, personality disorders, anxiety disorders, and major depression were 95, 45,
62 and 43 percent respectively [23]. Additional major psychiatric diagnoses included schizoaffective
disorder, bipolar disorder, and substance abuse.
In a case-control study, 64 adult patients with PMD 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) [24]. In addition, patients with PMD 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 PMD and healthy control groups.
CLINICAL FEATURES A number of clinical characteristics (table 4) are associated with PMDs [6,25]:

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Abrupt onset
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 'History and
examination' below)
Coactivation sign of antagonist muscles (see 'Psychogenic tremor' below and 'Electrodiagnostic
testing' below)
Deliberate slowness of movement
Association with false 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 PMD syndromes are psychogenic tremor, psychogenic dystonia, psychogenic gait, psychogenic
myoclonus, and psychogenic parkinsonism. These are reviewed in the sections below.
Psychogenic tremor Psychogenic tremor is the most common type of PMD [28]. (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). Psychogenic tremor is typically a complex resting, postural,
and action tremor. The only known organic tremor with such physical findings is a cerebellar outflow tremor (ie,
Holmes tremor) [29]. Any body part may be involved with psychogenic tremor, but hand tremor, leg tremor, and
whole body tremor are common sites [30]. Remarkably, the fingers are often spared with much of the upper limb
tremor occurring at the wrist [20,31].
A characteristic that suggests psychogenic tremor rather than organic tremors is abrupt onset with immediate
maximal severity, often precipitated by trivial emotional or physical trauma [28]. In contrast, essential tremor
typically begins gradually in one or both arms, requiring years to decades to worsen sufficiently to warrant
treatment (see "Overview of tremor"). With psychogenic 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 psychogenic tremor, restraining the affected limb may precipitate tremor in other previously
unaffected body regions. Additionally, the affected limb may "fight" with the examiner when it is restrained. The
coactivation sign describes the ongoing isometric contraction of antagonistic muscles that may be perceived on
examination as increased muscle tone during passive movement [31].
Electrophysiologic studies may be helpful in documenting the frequency of the psychogenic tremor and
distractibility. (See 'Electrodiagnostic testing' below.)
Psychogenic dystonia Psychogenic dystonia is the second most common type of PMD in most series (see
'Epidemiology' above).
True dystonia is defined as involuntary sustained muscle contractions causing twisting and repetitive movements
or abnormal postures (see "Classification and evaluation of dystonia"). Psychogenic dystonia may affect any part
of the body or be generalized. Features that suggest a psychogenic 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 [5,32,33]. Additional suggestive features include foot dystonia in an adult, the
presence of other atypical movements or postures such as a bizarre gait, 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 psychogenic dystonia due to disuse or prolonged maintenance of the tonic posture. Muscle

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hypertrophy may be present due to sustained contracture.

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 posttraumatic dystonia,
posttraumatic cervical dystonia, posttraumatic painful torticollis, peripherally induced dystonia, causalgiadystonia syndrome, and complex regional pain syndrome dystonia [18,34-40]. The inciting injury may involve
nerve root, peripheral nerve, or soft tissue. Although the mechanism of peripherally induced dystonia is
controversial [41-47], there is little evidence to support an organic basis, while the overlap with features
suggestive of PMD is extensive [35]. Thus, many cases are probably psychogenic.
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 [18]. 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. Psychogenic 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 psychogenic 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 posttraumatic painful dystonia, all 16 were seeking
compensation through the courts [34]. Unlike other forms of PMD, 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.
Psychogenic gait In psychogenic gait disorders, walking is often bizarre and does not conform to any of the
usual patterns observed with neurologic gait disorders (see "Gait disorders of elderly patients", 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
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19 century to describe certain patients with a frankly psychogenic gait [48,49]. 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 [5,50].
Features suggestive of a psychogenic gait disorder are illustrated by the following observations:
In a report that analyzed the clinical manifestations of psychogenic gait disorder in 37 patients, the
following six characteristics were identified as supporting the diagnosis [51]:
Momentary fluctuations of stance and gait, often in response to suggestion
Excessive slowness or hesitation of locomotion incompatible with neurologic disease
A "psychogenic" response to the Romberg test, with a build-up of swaying amplitudes after a silent
latency, or with improvement by distraction

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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 PMD, a psychogenic gait disturbance was
paired with additional psychogenic movements in 102 patients (37 percent), and a pure psychogenic gait
disturbance in 16 patients (5 percent) [52]. Thus, a psychogenic gait was present in a total of 118 patients
(42 percent). The most frequent gait patterns among all 118 patients with a psychogenic 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 psychogenic 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 PMD and normal gait, those with a psychogenic 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 psychogenic etiology. A cautious gait may be a
legitimate psychological adaptation, based upon an appropriate response to real or perceived disequilibrium [53].
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 [54]. However, other psychogenic features are typically absent [50]. In addition to appropriate caution and
fear of falling, the differential diagnosis of cautious gait includes higher level organic gait disorders. (See "Gait
disorders of elderly patients", section on 'Frontal lobe dysfunction'.)
Anxiety and depression usually have a minor effect on gait [49]. However, severely depressed patients with
psychomotor retardation may walk with reduced stride length and a lifting motion of the legs [55].
Psychogenic 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"). The characteristics of
psychogenic myoclonus were described in detail by a report of 212 patients with myoclonus that included 18
patients diagnosed with psychogenic myoclonus [56]. The characteristics of psychogenic myoclonus were the
following:
Inconsistent character of the movements (amplitude, frequency, and distribution) and other features
incongruous with typical "organic" myoclonus
Associated psychogenic 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
Electrodiagnostic testing can be helpful in differentiating psychogenic myoclonus from true myoclonus. (See
'Electrodiagnostic testing' below.)
Startle syndromes Startle is a physiologic generalized myoclonic response to an unexpected auditory,
visual, somatosensory, and 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 [57,58]. 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 [58,59]. Patients with
psychogenic startle tend to have an exaggerated initial startle response that habituates to repetitive stimulation
but shows inconsistent latencies [60].

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Culturally determined forms of startle presumed to be psychogenic in origin include the latah syndrome of
Malaysia and Indonesia, the Jumping Frenchmen of Maine, the Ragin' Cajuns of Louisiana, and the myriachit
phenomenon of eastern Siberia [61-63]. 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 [61].
Psychogenic 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 psychogenic parkinsonism can be superficially similar but have
features suggesting a psychogenic origin (see 'Clinical features' above).
Unlike a parkinsonian tremor, the tremor of psychogenic parkinsonism shares the characteristics of isolated
psychogenic tremor (see 'Psychogenic tremor' above), manifesting as a complex resting, postural, and action
tremor with abrupt onset, a static course, and changeable features [5,64-66]. The tremor will typically increase
with attention and decrease with distraction [30]. With psychogenic 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 (ie, gegenhalten) 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 psychogenic parkinsonism may coexist with organic Parkinson disease, and some evidence
suggests that psychogenic parkinsonism or other somatoform disorders can be an early manifestation of
Parkinson disease [67,68].
In a study of 14 patients with psychogenic parkinsonism, tremor was present in 12, balance and gait
difficulties were present in 12, and rigidity with voluntary resistance was noted in 6 [65]. Non-physiologic
weakness and sensory disturbances were present in 10 patients.
In another report of nine patients referred for suspicion of psychogenic parkinsonism who were followed
for at least two years, the final diagnosis was pure psychogenic parkinsonism for four patients and a
combination of psychogenic parkinsonism with Parkinson disease for five patients [69]. 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 psychogenic 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 psychogenic parkinsonism.
A normal dopamine transporter imaging study using SPECT scan is helpful for supporting a diagnosis of
psychogenic, drug-induced or vascular parkinsonism [70]. However, change from normal to abnormal may occur
over time, and, therefore, a single test should not be used to support a diagnosis of PMD. (See
'Neuroimaging' below and "Diagnosis of Parkinson disease", section on 'DaTscan'.)
DIAGNOSIS AND DIFFERENTIAL The diagnosis of a PMD is based upon clinical impression:
The diagnosis of PMD requires the presence of characteristic clinical features (table 4), particularly
symptoms and signs that are inconsistent over time and incongruent with organic movement disorders
[1,6]. 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 PMD,
but their presence is not required [14].
PMD can coexist with organic illness.

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There is no gold standard test for confirming the diagnosis of PMD. However, electrodiagnostic studies
can provide additional supportive evidence for the diagnosis of psychogenic tremor and psychogenic
myoclonus, and dopamine transporter imaging with SPECT scan can support the diagnosis of
psychogenic parkinsonism by excluding organic causes of parkinsonism. (See 'Electrodiagnostic
testing' below and 'Neuroimaging' below.)
The diagnosis of PMD 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 PMDs, 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
psychogenic parkinsonism. In fact, such a presentation is common among other parkinsonian syndromes such
as multiple system atrophy. (See "Multiple system atrophy: Clinical features and diagnosis".)
Among PMDs, psychogenic dystonia is particularly challenging to diagnose because it is typically a persistent,
tonic condition that often manifests as a fixed posture [6]. These features contrast with the variability that is
typical of most other PMDs. In addition, they preclude assessment of certain clues that support a psychogenic
etiology, such as distractibility, entrainment, and increased movement during observation or examination.
As a note of caution, the literature documents a number of examples of mislabeling PMD [9,10,71]. 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 [72].
While not specific for PMDs, this finding suggests that the misdiagnosis rate for conversion disorder is not
unacceptably high compared with other psychiatric and neurologic disorders [73].
History and examination PMDs often begin suddenly with maximal disability at onset after a trivial
provocation (eg, lifting a moderate weight, or following a non-concussive motor vehicle accident). In contrast,
organic movement disorders typically begin gradually, 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.
Despite severe disability, PMD 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 psychogenic etiology of a movement disorder; for example,
complete remission of parkinsonian symptoms with herbal remedies [74]. Similarly, lack of response to
appropriate treatment, such as levodopa for Parkinson disease, also increases suspicion for PMD in the proper
clinical context [64]. However, this is a nonspecific finding that could also support a diagnosis of atypical
parkinsonism.
Social history may provide important clues to PMD. Familiarity with organic illness among family members,
acquaintances, or due to employment as a healthcare professional, may predispose to the development of PMD.
A history of sexual or physical abuse may be suppressed by patients with PMD and should be considered
carefully when interviewing the patient [75]. 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.
Accompanying signs or symptoms are helpful in diagnosing PMD. Nonanatomic sensory change, give-way
weakness, and bizarre gaits (eg, walking on a tightrope, histrionic lurching without losing balance) are common
in PMD [52]. Patients may have nonphysiologic triggers or relieving factors (eg, tapping the patellar tendon,
inducing distant myoclonus or squeezing the neck, inducing forceful neck flexion).
One of the most important physical findings that can help differentiate PMD 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 PMD. In contrast, distracting
maneuvers usually increase intensity of the movement in organic movement disorders. Variation in frequency

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and amplitude of the movement, especially with tremor, is an additional clue that the movement is psychogenic.
Entrainment is another feature associated with PMD, and refers to the physical examination finding of the limb
taking on the same frequency of movement as an unaffected limb during a maneuver requiring concentration. In
particular, psychogenic tremor will entrain (take on the distracting maneuver's frequency) 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 PMD [76].
Electrodiagnostic testing Electrodiagnostic methods can provide additional supportive evidence for the
diagnosis of psychogenic tremor and psychogenic myoclonus. However, electrodiagnostic methods for analyzing
tremor and myoclonus are not universally available and depend on patient effort for accuracy.
Tremor analysis using surface electromyography (EMG) and accelerometry can identify features associated with
psychogenic tremor, including entrainment, coactivation of antagonist muscles, variability in tremor frequency,
and increased tremor amplitude and frequency with weight loading of the involved limb [25,31,76,77]. Coherence
analysis is a quantitative method to determine the similarity of tremor oscillation frequency and phase in different
limbs or body parts. Psychogenic tremor typically has the same frequency in different limbs or in the shaking limb
and another limb performing distracting maneuvers [78]. 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 [79].
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 an organic etiology of tremor, since essential
tremor and parkinsonian tremor maintain their original frequencies and do not entrain. However, in some cases
psychogenic tremor will stop or change frequency rather than show clear entrainment. In longstanding PMD,
distracting maneuvers may not be effective, a feature that limits the utility of testing with electrodiagnostic
methods such as an accelerometer [76].
Electrodiagnostic techniques, including surface EMG, electroencephalography (EEG), back-averaged EEG, and
somatosensory evoked potentials, can be helpful in differentiating psychogenic myoclonus from true myoclonus.
Features associated with psychogenic 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 [80,81]. 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 psychogenic myoclonus. In
addition, psychogenic 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 [82].
There are no definitive electrodiagnostic tests for distinguishing psychogenic dystonia from organic dystonia [79].
Neuroimaging A normal dopamine transporter imaging study using SPECT scan is helpful for supporting a
diagnosis of psychogenic, drug-induced or vascular parkinsonism [70]. However, change from normal to
abnormal may occur over time, and, therefore, a single test should not be used to support a diagnosis of PMD.
(See "Diagnosis of Parkinson disease", section on 'DaTscan'.)
Neuroimaging with CT and MRI scans has little utility for the diagnosis of patients with suspected PMD, except to
exclude the possibility of an underlying structural abnormality that potentially contradicts the diagnosis of a PMD.
However, the diagnosis of PMD depends on positive criteria (table 4) and is not merely one of exclusion.
Classification of diagnostic certainty Criteria for degrees of certainty in the diagnosis of PMDs were first
proposed in 1988 and are well-known among specialists familiar with PMDs [32]:
Documented PMD Consistently and persistently relieved by psychotherapy with or without psychotropic

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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 PMD Inconsistent symptoms and signs, and presentation incongruent with the
typical presentation of an organic movement disorder, and presence of other psychogenic signs such as
false weakness or sensory loss, multiple somatizations and obvious psychiatric diagnosis.
Probable PMD Inconsistent or incongruent with an organic movement disorder but lacking other
features listed above, or abnormal movements that are consistent and congruent with an organic disorder
and coexistent psychogenic signs such as false weakness or sensory loss, or movements consistent and
congruent with an organic disorder but manifest multiple somatizations.
Possible PMD Movements consistent and congruent with an organic disorder, but other features are
present that raise the level of suspicion that the diagnosis is psychogenic 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 [1,14,83], but the clinical
value of the original and revised versions is uncertain [73].
MANAGEMENT Optimal management of PMDs 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 PMD is often problematic because most
patients do not accept that the trouble may be psychiatric, and many become alienated and seek another opinion
[11]. However, it is the role of the neurologist to make and convey the diagnosis of PMD because most
psychiatrists lack sufficient expertise in movement disorders. While some experts use the term psychogenic
when telling the patient of the diagnosis of PMD, others suggest that the term functional movement disorder
may be preferred for patient acceptance. Except for rare patients with factitious disorder or malingering, it is
important to let the patient know that the condition is real and involuntary, that the main components of the
neurologic examination are normal, and that there is potential for recovery [5,11]. Some neurologists find it useful
to review symptoms with the patient using a website www.neurosymptoms.org that 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 [84].
It is also advisable to tell the patient that the best approach to treatment involves the neurologist working with a
psychiatrist or other practitioner who is skilled in psychological counselling and familiar with PMDs [11,85].
Treatment options There are no proven or universally accepted treatments for PMDs. The evidence
supporting available treatments mainly comes from small retrospective studies, and large randomized controlled
trials are lacking [5]. Treatments that may be helpful include psychotherapy with or without pharmacotherapy
[85], cognitive behavioral therapy [86], physical therapy [87,88], antidepressant medications [89], mild to
moderate exercise [90], transcranial magnetic stimulation [91], and hypnosis [92]. Psychiatric interventions are
individualized according to the underlying psychiatric diagnosis. (See 'Underlying psychiatric disorders' above.)
Multidisciplinary inpatient treatment of PMD 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 [93]. In an observational study that prospectively followed 42 patients with fixed dystonia, most of whom
fulfilled criteria for PMD 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 [18]. These uncontrolled data suggest but do not prove that a
multidisciplinary inpatient treatment approach is effective for PMD. However, inpatient treatment for PMD is
generally not a viable option in the United States due to insurance restrictions.
A few small uncontrolled prospective studies have evaluated the treatment of PMD, as illustrated by the following
observations:

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An assessor-blinded study of nine patients with PMD reported that 12 weeks of psychotherapy was
associated with a statistically significant improvement in movement disorder severity compared with
baseline [85].
In an uncontrolled study of 15 patients with chronic PMD and recent or current depression or anxiety,
antidepressant treatment was associated with improvement in most patients [89].
In another assessor-blinded study of 16 sedentary patients with PMD who were treated with a 12 week
program of exercise (low intensity walking three times a week), a statistically significant improvement in
movement disorder severity was reported for 10 patients (63 percent) [90].
However, the strength of these studies is limited by the small size and lack of control groups.
Given the available data and our clinical experience, we suggest multidisciplinary inpatient treatment (where
available) combining psychotherapy, cognitive behavioral therapy, physical therapy, and occupational therapy for
patients with PMD rather than outpatient treatment. We suggest multidisciplinary outpatient treatment using the
same modalities when inpatient treatment is not an option.
In our clinical experience, treatment includes disclosing the diagnosis (see 'Explaining the diagnosis' above) to
the patient with emphasis that the problem is not made up by the patient or in their head. PMDs represent the
complex interaction of mind and physical expression. Involvement with a psychiatrist or psychologist who is
familiar with PMDs and treatment of underlying anxiety and depression are useful. Engaging physiotherapy to
improve function gradually in a safe environment can be helpful. Finally, 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 PMD. 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
patients 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 PMD is generally poor [11,23,94]. In one
prospective study of 42 subjects with PMD who were followed for a mean of three years, abnormal movements
persisted in 90 percent [23]. In a retrospective study with self-reported outcome data for 122 patients with PMD
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 [26].
Although data are limited, the following factors have been associated with a poor prognosis for PMD [23,26]:
Long duration of illness
Insidious onset of symptoms
Inconsistency of movements
Psychiatric comorbidity
Smoking
Suggestibility
Dissatisfaction with physician
Factors associated with a more favorable PMD prognosis include the following [23,26]:
Short duration of symptoms (<1 year)
Good physical health
Positive social life perception
Elimination of stressors
Patient perception of receiving effective treatment
The presence of litigation did not correlate significantly with prognosis in these studies [23,26].
SUMMARY AND RECOMMENDATIONS
Psychogenic movement disorder (PMD) is a clinical syndrome defined as the occurrence of abnormal
movements that result from a psychologic or psychiatric cause rather than a medical or neurologic cause.

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Alternative terms for PMD include hysterical movement disorder, functional movement disorder,
nonorganic movement disorder, and medically unexplained motor symptoms. (See 'Introduction and
background' above.)
Prevalence estimates among adults and children suggest that PMDs account for 2 to 4 percent of all
movement disorders. Psychogenic tremor is the most frequent type of involuntary movement with PMD,
followed by psychogenic dystonia. (See 'Epidemiology' above.)
Conversion disorder (table 1) is probably the most common mechanism of PMD. (See 'Underlying
psychiatric disorders' above.)
A number of clinical characteristics (table 4) are associated with PMDs. The main PMD syndromes are
psychogenic tremor, psychogenic dystonia, psychogenic gait, psychogenic myoclonus, and psychogenic
parkinsonism.
Psychogenic 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 'Psychogenic tremor' above.)
Psychogenic 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 'Psychogenic dystonia' above.)
Dystonia that occurs after peripheral trauma is known by a number of terms, including fixed dystonia,
traumatic or posttraumatic dystonia, posttraumatic cervical dystonia, posttraumatic painful torticollis,
peripherally induced dystonia, causalgia-dystonia syndrome, and complex regional pain syndrome
dystonia. Although controversial, many cases are probably psychogenic. (See 'Peripherally induced
dystonia' above.)
In psychogenic gait disorders, walking is often bizarre and does not conform to any of the usual
patterns observed with neurologic gait disorders. (See 'Psychogenic gait' above.)
The characteristics of psychogenic myoclonus include features similar to other PMDs 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 'Psychogenic
myoclonus' above.)
The tremor of psychogenic parkinsonism shares the characteristics of isolated psychogenic tremor,
manifesting as a complex resting, postural, and action tremor with abrupt onset, a static course, and
changeable features. With psychogenic 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 'Psychogenic
parkinsonism' above.)
The diagnosis of PMD requires the presence of characteristic clinical features, particularly symptoms and
signs that are inconsistent over time and incongruent with organic movement disorders (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
psychogenic tremor and psychogenic myoclonus, and dopamine transporter imaging with SPECT scan
can support the diagnosis of psychogenic parkinsonism by excluding organic causes of parkinsonism.
(See 'Diagnosis and differential' above.)
There is no proven or universally accepted treatment for PMDs. Optimal management consists of early
diagnosis, providing the patient a credible explanation of the diagnosis, and a multidisciplinary approach
to treatment that combines psychotherapy, cognitive behavioral therapy, physical therapy, and

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occupational therapy. Some patients respond to pressure, suggestion, prayer and other nonconventional
interventions. (See 'Management' above.)
Prognosis for complete remission with longstanding PMD is generally poor. However, a number of factors
are associated with a more favorable prognosis, including short duration of symptoms, good physical
health, positive social life perception, elimination of stressors, and patient perception of receiving effective
treatment. (See 'Prognosis' above.)

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Topic 14132 Version 6.0

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GRAPHICS
DSM-IV-TR diagnostic criteria for conversion disorder
A. One or more symptoms or deficits affecting voluntary motor or sensory function that suggest
a neurological or other general medical condition.
B. Psychological factors are judged to be associated with the symptom or deficit because the
initiation or exacerbation of the symptom or deficit is preceded by conflicts or other stressors.
C. The symptom or deficit is not intentionally produced or feigned (as in Factitious Disorder or
Malingering).
D. The symptom or deficit cannot, after appropriate investigation, be fully explained by a general
medical condition, or by the direct effects of a substance, or as a culturally sanctioned behavior
or experience.
E. The symptom or deficit causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning or warrants medical evaluation.
F. The symptom or deficit is not limited to pain or sexual dysfunction, does not occur exclusively
during the course of somatization disorder, and is not better accounted for by another mental
disorder.
Specify type of symptom or deficit:
With motor symptom or deficit
With sensory symptom or deficit
With seizures or convulsions
With mixed presentation

Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Text Revision,
Fourth Edition. Copyright 2000 American Psychiatric Association.

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Somatization
A. Somatoform disorders
1. Somatoform disorders common to the American Psychiatric Association's Diagnostic and
Statistical Manual, Fourth Edition, Text Revision (DSM-IV-TR) and World Health Organization's
International Classification of Diseases-10th Revision (ICD-10)
a. Somatization disorder
b. Undifferentiated somatoform disorder
c. Pain disorder
d. Hypochondriasis
e. Somatoform disorder not otherwise specified

2. Somatoform disorders unique to DSM-IV-TR

a. Conversion disorder
b. Body dysmorphic disorder

3. Somatoform disorders unique to ICD-10

a. Somatoform autonomic dysfunction
b. Other somatoform disorders

B. Other specific types of somatization common to DSM-IV-TR and

ICD-10
1. Factitious disorder
2. Malingering

Additional categories have been proposed that are not recognized by

DSM-IV-TR or ICD-10, to address dissatisfaction with existing
diagnoses. These categories are:
1. Abridged somatization
2. Multisomatoform disorder
Adapted from:
1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition,
Text Revision. Washington, DC, American Psychiatric Association, 2000.
2. World Health Organization. International Statistical Classification of Diseases and Related Health
Problems, 10th Revision, Version for 2007. http://www.who.int/classifications/apps/icd/icd10online/
(Accessed on November 22, 2009).

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General diagnostic criteria for personality disorder

DSM-IV requires that the following be present in order to diagnose a
personality disorder:
A. An enduring pattern of inner experience and behavior that deviates markedly from the
expectations of the individual's culture. This pattern is manifested in two (or more) of the
following areas:
1. Cognition (ie, ways of perceiving and interpreting self, other people, and events)
2. Affectivity (ie, the range, intensity, lability, and appropriateness of emotional response)
3. Interpersonal functioning
4. Impulse control

B. The enduring pattern is inflexible and pervasive across a broad range of personal and social
situations.
C. The enduring pattern leads to clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
D. The pattern is stable and of long duration and its onset can be traced back at least to
adolescence or early adulthood
E. The enduring pattern is not better accounted for as a manifestation or consequence of another
mental disorder
F. The enduring pattern is not due to the direct physiological effects of a substance (eg, a drug of
abuse, a medication) or a general medical condition (eg, head trauma)
Adapted from American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th
ed, Text revision (DSM-IV-TR). American Psychiatric Association, Washington, DC, 2000.

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Clinical characteristics of psychogenic movement disorders

Abrupt onset
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 abnormal movements 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
Coactivation sign of antagonist muscles
Deliberate slowness of movement
Association with false weakness, sensory loss, and pain
Functional disability out of proportion to exam findings
Unresponsiveness to drugs for organic movement disorders
Response to placebo drugs and suggestion

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Common tremors
Resting tremor
Parkinson disease
Parkinsonian syndromes
Midbrain (rubral) tremor
Wilson's disease
Severe essential tremor

Postural-action tremor
Enhanced physiologic tremor
Essential tremor
Primary writing tremor
Other extrapyramidal disorders
Parkinson disease
Wilson's disease
Dystonia

Cerebellar disease
Peripheral neuropathy

Intention tremor (cerebellar outflow)

Cerebellar disease
Multiple sclerosis
Midbrain stroke
Midbrain trauma

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