Hyperkinetic Movement Disorders Volume 25/1 || Psychogenic Movement Disorders

165O. Suchowersky and C. Comella (eds.), Hyperkinetic Movement Disorders, Current Clinical Neurology, DOI 10.1007/978-1-60327-120-2_7, © Springer Science+Business Media New York 2012

Introduction

Psychogenic movement disorders (PMDs) are defi ned as follows: “those movement disorders which cannot be fully accounted for by any known organic syndrome and which appear as based on available clinical evidence to have signifi cant psychological and/or psychiatric contributants” [ 1 ] and have been variously labeled as functional, pseudoneurologic, psychosomatic, hysterical, and nonorganic [ 2, 3 ] . PMDs can be either hyperkinetic, such as myoclonus, or hypokinetic, such as parkinsonism. This chapter deals with hyperkinetic PMDs, including tremor, dystonia, myoclonus, tic, chorea/athetosis, gait disorders, and exaggerated startle refl ex.

Chapter 7 Psychogenic Movement Disorders

Teri R. Thomsen and Janis M. Miyasaki

T. R. Thomsen , MD, JD University of Iowa Hospital and Clinic, Neurology 2 RCP, 200 Hawkins Drive , Iowa City , IA 52242 , USA

J. M. Miyasaki , MD, FRCPC (*) Department of Medicine (Neurology) , University of Toronto, The Movement Disorder Centre, 399 Bathurst Street, 7MCL , Toronto , ON , Canada M5T 2S8 e-mail: [email protected]

This chapter contains videos segment which can be found at the URL: http://www.springerimages.com/Suchowersky

Video Segment Content

Case 1: Psychogenic gait.Note the non-anatomic posture of the feet in extreme external rotation. Clinicians should be familiar with typical cerebellar gait (broad-based and irregular steps), parkinsonian (small steps with festination or freezing) and dystonic gait (postures will change with walking with occasional resolution of dystonic posture in feet with walking backwards). Unusual gaits should be reviewed: cock walking gait with manganese toxicity and the gait with neuroacanthocytosis. Case 2: Psychogenic tremor.Note the tremor is inconsistent in amplitude, direction and nature. Tremor is dis-tractible with conversation and also entrains with movements performed by other parts of the body requiring concentration. This feature may not be present when psychogenic tremor is present for long periods of time.

Also see Chapter 3, cases 21 and 22 and Chapter 6, cases 11 and 12.

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166 T.R. Thomsen and J.M. Miyasaki

PMDs are a signifi cant source of morbidity and disability in affected persons; therefore, a basic understanding of these disorders is important to allow neurolo-gists to recognize their presentation [ 4 ] . Estimates of the prevalence of PMDs range from 1 to 25% due to differing diagnostic criteria and ascertainment methodologies [ 4, 5 ] . One study noted that among 4,470 consecutive neurological inpatients, 405 of these (9%) were found to have a psychogenic disorder [ 6 ] ( Table 7.1 ).

In one movement disorder clinic, of 842 consecutive newly assessed patients, 28 (3.3%) were diagnosed with PMDs over a 71-month period [ 7 ] . Twenty-fi ve percent of these PMD patients had a coexisting organic movement disorder, and 71% had other psychogenic features, including give-way weakness and nonphysiologic sensory loss. A retrospective review of 14,568 patients assessed over a 15-year period at another clinic noted a 3.6% incidence of PMDs [ 5 ] . Transcultural compari-son between patient populations in Spain and the USA noted similar demographics, movement types, anatomical distribution, and functional impairment [ 8 ] . The age of onset of PMDs ranges from 4 to 73 years old, with a mean of 44 years [ 5 ] .

The societal burden of PMDs is potentially large. These patients have intense utilization of the healthcare system with more frequent offi ce visits, extensive and often expensive testing in a futile effort to fi nd any organic illness or to clarify previous tests with unclear results, specialist consultations, and often unnecessary procedures [ 9 ] . Estimates of additional healthcare costs associated with PMDs range from $20 to $100 billion per year [ 9, 10 ] . Monetary costs do not refl ect the impact of PMDs on patients’ quality of life. In addition, the cost of lost work days and disability compensation is considerable. Often, PMD patients will have ongoing lawsuits or worker’s compensation cases, and symptoms may improve following resolution of these legal matters. PMD patients may present with situa-tions where the fi nancial benefi t of being disabled is similar to that of a return to employment; this provides a disincentive to recovery [ 9 ] .

Care needs to be taken when making a diagnosis of PMD as a follow-up study of patients previously given the diagnosis of hysteria found that in 28 cases out of 85, an organic diagnosis was later found [ 11 ] . Another investigation found that organic disorders coexist in 10–15% of PMD patients [ 5 ] . Just as seizures and pseudoseizures coexist in a single patient, what appears unusual might distract from organic illness. Although a course of illness or development of the movement

Table 7.1 Prevalence of various PMDs noted in recent studies

Factor et al. [ 4 ]

Thomas et al. [ 2 ]

Miyasaki et al. [ 1 ]

Williams et al. [ 15 ]

Tremor (%) 50 39.8 32.8 13 Dystonia (%) 18 40.6 25 53 Myoclonus (%) 14 17.2 25 7 Parkinsonism (%) 7 3.2 6.1 1.9 Tic (%) 4.3 1.3 Chorea (%) 0.6 Other dyskinesia (%) 10 1.5 9 Gait disorder (%) 10.9 9

1677 Psychogenic Movement Disorders

disorder that is atypical for an organic illness serves as one clue to PMD, the description of new illnesses should serve as cautionary tales for the neurologist. A typical course of Parkinson’s disease is a gradual onset over months to years. Yet, rapid onset parkinsonism dystonia is recognized as a true illness [ 12 ] . Therefore, the possible errors in diagnosing these patients include discounting organic disease as somatoform thereby denying appropriate therapy or labeling somatoform disorders as organic, thereby enforcing the sick role. Increasing awareness of psychogenic illnesses led to the involvement of neurologists, among other physicians, in the diagnosis and management of these disorders [ 11 ] .

The presentation of psychogenic illness changes over time and refl ects deeper cultural trends. For example, pseudoepilepsy was common in the seventeenth and eighteenth centuries, while functional muscle paresis and paralysis rose in the nineteenth century [ 2 ] . The underlying cause, to which patients ascribe their ill-nesses, also changes with time, for instance, pseudoepilepsy was attributed to demonic possession several centuries ago. Since PMDs often depend on a model for the movements, internet use, providing rapid dissemination of information, both written and visual, might contribute to an increase in PMDs [ 13 ] .

The main approach to diagnosis of psychogenic disorders involves clinical examination and observation, using as much ancillary evidence as possible, such as response to placebo drugs and suggestion, and negative results of investigative test-ing (such as, MRI, functional neuroimaging, neurophysiologic testing, psychiatric diagnosis) [ 4, 10 ] . In diagnosing PMDs as organic, the patient is exposed to unnec-essary investigations and therapy that entail risk and side effects (ranging in severity from a nuisance to potentially fatal, such as deep brain stimulation) [ 4, 14 ] . Further, over-investigation causes stronger assumption of the sick role, minimizing the like-lihood of remission [ 15 ] . In contrast, diagnosing organic illness as PMD may deny treatment that can signifi cantly improve their quality of life or affect workplace accommodation of their disability [ 1, 4 ] .

Psychiatric Diagnoses Common in PMDs

The term psychogenic implies that there is no organic basis to the illness and that the symptoms are a manifestation of an underlying psychiatric process or diagnosis [ 3, 16 ] . When a patient presents with symptoms likely to be of psychological origin, there are several possibilities. The symptoms may be due exclusively to a psychiat-ric disorder, an aspect of the presentation of another psychiatric disorder (such as depression or anxiety), an expression of a psychiatric disorder that is linked to an organic disorder (such as depression in Parkinson’s disease), or manifestations of an unusual clinical presentation of a physical disorder [ 16 ] . Extensive clinical experi-ence and familiarity with typical presentations and physical examination fi ndings of organic movement disorders is required in order to establish a diagnosis of PMD.

As the term psychogenic is vague and does not specify an exact psychiatric diagno-sis, several psychiatric diagnoses are commonly covered by the umbrella term PMDs.


These include somatoform disorders, factitious disorder, malingering, depression, anxiety, and histrionic personality disorder [ 4, 9, 16 ] .

As set forth in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition [ 17 ] , somatoform disorders include the following: somatization disorder (previously termed hysteria or Briquet’s syndrome), undifferentiated somatoform disorder, conversion disorder, pain disorder, hypochondriasis, body dysmorphic dis-order, and somatoform disorder not otherwise specifi ed [ 18 ] . The hallmark of soma-toform disorders is the presence of symptoms suggestive of a medical illness, but not fully explained by a medical condition or by the effects of a substance or other mental disorder [ 1, 17, 18 ] . The symptoms must cause signifi cant distress or result in impairment of social, occupational, or other areas of functioning. As compared to factitious disorders and malingering, the symptoms in somatoform disorders are not intentionally produced or feigned [ 15 ] .

Somatization disorder is characterized by multiple symptoms, including pain, gastrointestinal, sexual, and pseudoneurological symptoms, initially occurring prior to age 30 and extending over a period of multiple years [ 9, 15, 18 ] . Undifferentiated somatoform disorder is diagnosed when the patient has unexplained physical symp-toms, lasting at least 6 months, that do not reach the threshold for a diagnosis of somatization disorder [ 15 ] . Conversion disorder is marked by symptoms affecting voluntary movement or sensory function that are suggestive of a neurological or other medical condition such as being paralyzed, yet able to move voluntarily dur-ing portions of the examination not specifi cally related to motor testing [ 4, 9, 15 ] . Pain disorder is characterized by the occurrence of pain as the predominant focus of clinical attention, with psychological factors playing a major role in the onset, sever-ity, exacerbation, or maintenance of pain. Hypochondriasis consists of the preoc-cupation with the fear of having, or the idea that one has, a serious illness based on one’s misperception of bodily symptoms or functions [ 15 ] . An example would be believing one has a brain tumor when experiencing a tension-type headache. Body dysmorphic disorder is characterized by the preoccupation with an imagined or exaggerated defect in physical appearance. Somatoform disorder not otherwise specifi ed is a term coined to designate those somatoform symptoms not meeting the criteria of the other somatoform disorders listed previously. With all of the above disorders, onset or exacerbation of symptoms is associated with stressors. In all somatoform disorders, the symptoms are not under voluntary control [ 4, 9 ] .

In contrast, factitious disorder and malingering are characterized by the volitional nature of the production of symptoms [ 4, 9 ] . In factitious disorder, the symptoms are consciously produced for psychological benefi t, in order to assume the sick role. The fi rst criterion in the diagnosis of factitious disorder is that the physical or psychologi-cal signs or symptoms be intentionally produced [ 15 ] . This may include fabrication of a subjective complaint (stomach pain), an objective sign (heating a thermometer to show a fever), self-infl icted conditions (injecting feces intravenously or aspirating feces), exaggeration or exacerbation of preexisting medical conditions (feigning a seizure), or some combination thereof. The second criterion is that the motivation for the behavior is to assume the sick role. The third criterion is an absence of exter-nal incentives for the behavior to separate this from malingering. Patients with facti-tious disorders tend to be overly dramatic, but vague on details [ 15 ] . They may


engage in pathological lying, accumulate extensive medical knowledge, and be willing to undergo multiple invasive procedures. If their ruse is discovered, these patients typically deny or avoid the allegations and will seek medical care from another practitioner or facility. One must exclude the possibility that the symptoms are real, as in a true medical condition, or that the symptoms are unconsciously pro-duced, as in a somatoform disorder, before diagnosing factitious disorder.

In malingering, the symptoms are intentionally produced for external gain, to avoid responsibility or obtain compensation [ 4, 9, 15 ] . The symptoms are either false or grossly exaggerated physical or psychological symptoms. Malingering is motivated by external incentives, which may include the production of symptoms to avoid jury duty, work, standing trial, or military duty; to obtain fi nancial compensation; or to obtain drugs. Exacerbation of a mental illness to avoid transfer to another less desir-able facility would also fall into this category. Malingering should be suspected in the following contexts: discrepancy between objective fi ndings and claimed disability, lack of cooperation with examination and recommended treatment, and the presence of antisocial personality disorder. The PMD may be the basis for legal action where substantial monetary gain is expected. As previously noted, malingering is distin-guished from conversion disorder and other somatoform disorders by the intentional production of symptoms and the presence of external incentives. In contrast to conver-sion disorder, relief of symptoms is not obtained by suggestion or hypnosis in malin-gering [ 15 ] . Rather, relief of symptoms may coincide with achievement of the external gain, such as settling a lawsuit or when the patient is not aware of observation. Video surveillance may be the strongest corroborating factor in malingering [ 9 ] .

Personality disorders, such as histrionic personality disorder, borderline person-ality disorder, and antisocial personality disorder, may predispose to the develop-ment of PMDs [ 4 ] . A personality disorder is characterized by a pattern of inner experience and behavior that deviates markedly from the expectations of an indi-vidual’s culture, is pervasive and infl exible, has onset in adolescence or early adult-hood, is stable over time, and causes impairment or distress [ 15 ] . As noted above, antisocial personality disorder may be associated with malingering. Antisocial per-sonality disorder is characterized by a pattern of disregard for, and the violation of, the rights of others. Borderline personality disorder is most frequently associated with factitious disorder. Borderline personality disorder is characterized by a pat-tern of instability in interpersonal relationships, self-image, fl uctuating affect, and marked impulsivity. It is further characterized by anxiety that the patient disperses by emotional lability directed at others. Histrionic, borderline, dependant, and anti-social personality disorders are most frequently associated with somatization disor-der and conversion disorder. Histrionic personality disorder is marked by a pattern of grandiosity, the need for admiration, and a lack of empathy. Dependant personal-ity disorder is characterized by a pattern of submissive and clinging behavior related to an excessive need to be taken care of. Antisocial and borderline personality dis-orders may tend to become less evident or remit with age, but other personality disorders tend to persist lifelong. The diagnosis of a personality disorder requires a prolonged period of assessment, often over months if not years. Therefore, a psychiatric therapeutic relationship shorter than this cannot defi nitely state that a personality disorder is not present in the PMD patient.


Features Suggestive of PMDs

To diagnose PMDs, one must have excellent knowledge of the typical course and fi ndings on physical examination of organic movement disorders. Therefore, a history inconsistent with the known organic counterpart is supportive. In general, movement disorders have a gradual onset. For instance, with dystonia, the abnormal posture begins intermittently, often with activity or movements involving the affected limb. Over time, the posture becomes more frequent and more severe. In the case of cervical dystonia, the neck turning may begin with walking and be mild and easy to overcome. Over the course of months, neck turning may occur while sitting or reading, be more extreme so that the head cannot be brought past midline and sensory tricks no longer afford relief. Therefore, presentation with onset of a fi xed abnormal neck posture appearing over minutes or days is suspicious for PMD.

Similarly, movement disorders do not have spontaneous remissions with days or weeks not affected by the movement, only to have disability reappear spontane-ously. Patients may be observed surreptitiously to have completely normal function, only to appear in the doctor’s offi ce unable to independently ambulate. Such observational opportunities are less available to the physician since hospital admissions are now rare or brief for PMDs. Video surveillance may be used in the diagnosis of PMD. However, this tool is often not available to physicians. Many patients with PMDs do submit their own “home” videos to demonstrate their disability. These may offer clues to PMD diagnosis due to inconsistency in movements, bizarre nature, or striking paroxysmal nature.

Historical features associated with PMDs include the following: abrupt onset, static course, spontaneous remissions (inconsistency over time), obvious psychiatric disturbance, multiple somatizations, pending litigation or compensation, presence of secondary gain, employment in a health profession, and young female patients [ 4 ] (Table 7.2 ).

A patient reporting abrupt onset of an abnormal movement may be suffering from a PMD, especially if the precipitating event was emotionally charged, such as a death in the family or a physical assault on the patient. Relatively benign events may precipitate PMDs in persons with poor coping skills, including such minor injuries as bumps, scrapes, and bruises [ 9, 10 ] . One study of 28 patients with PMDs noted that 17 patients (61%) had a precipitating event, including work-related injuries, motor vehicle and other accidents, exposure to potential toxins, and surgery [ 7 ] . Of these patients, 7 submitted workman’s compensation claims, 6 fi led personal injury lawsuits, and 1 patient had onset of dystonia in court to avoid prosecution.

PMDs commonly coexist with signifi cant psychiatric diagnoses. One study noted that 38% of PMD patients carried an Axis I diagnosis (typically depression and anxiety disorder) (Diagnostic and Statistical Manual of Mental Disorders, fourth edition, DSM-IV [ 17 ] ), and 42% of patients carried an Axis II diagnosis (personality disorder), in addition to a diagnosis of conversion disorder [ 19 ] . Fifty percent of PMD patients were noted to have a psychiatric diagnosis in the study of 842 patients discussed previously [ 7 ] . Common psychiatric diagnoses accompanying PMDs


include the following: major depression, anxiety disorders (obsessive compulsive disorder, panic disorder, phobia, generalized anxiety disorder), personality disorders (histrionic personality disorder, borderline personality disorder, dependant person-ality disorder, and antisocial personality disorder), substance abuse, somatoform disorders, and conversion disorders [ 19 ] . Anxiety contributing to excessive concern about normal fl uctuations in bodily function is highly plausible for many patients. Further, treatment of anxiety can markedly improve their physical status [ 20 ] .

An atypical course of illness, such as a fast progression to maximum symptom severity or conversely a static course in an illness such as parkinsonism where progression is expected, is suggestive of PMD, as do paroxysmal symptoms and spontaneous remissions and relapses [ 9, 10 ] . Psychogenic symptoms may modulate over time, such as numbness switching to involve a different side of the body. Selective disability is a hallmark of psychogenic disorders, as is disability out of proportion to the visible disorder.

One PMD may occur in combination with other PMDs, such as tremor occurring with dystonia and a gait disorder [ 6 ] . Also of note, PMDs tend to occur in the context of multiple somatizations, such as visual problems, memory loss, and gastrointestinal complaints [ 9 ] . Other features on neurologic exam include a non-anatomic distribution of sensory loss, hemisensory loss, or a nonorganic pattern of weakness. PMDs may be associated with organic movement disorders in up to 15% of patients [ 10 ] .

Clues to PMD include not only occupation but also exposure to “models” for PMD, for example, the patient with psychogenic dystonia whose cousin has cerebral palsy or the patient with psychogenic tremor whose father was recently diagnosed with Parkinson’s disease. Thus, healthcare providers such as nurses and allied health professionals have ample exposure to potential models for their “illness” and frequently present with PMD [ 4, 5 ] . Despite advances in equality in the workplace and society, nearly 100 years since the fi rst diagnosis of hysteria, women continue to comprise the majority of PMD sufferers (61–87% of cases).

Table 7.2 Clinical features associated with PMDs [ 1, 11 ]

Inconsistent character of the movement (amplitude, frequency, distribution, selective disability) Abrupt onset, paroxysmal in nature, or periods of spontaneous remission Movements that increase with attention or decrease with distraction Ability to trigger or relieve the abnormal movements with unusual or nonphysiological

intervention (e.g., trigger points on the body, application of a tuning fork) False weakness False sensory complaints Self-infl icted injuries Deliberate slowness of movements Functional disability out of proportion to exam fi ndings Movement abnormality that is bizarre, multiple, or diffi cult to classify Atypical response to a pharmacological agent Astasia-abasia Entrainment of tremor to the frequency of repetitive movements Co-contraction sign in tremor


Patients often present with multiple investigations and repetitions of investigations. Further, multiple consultations with physicians or complementary health practitioners are common. Schrag and Lang [ 21 ] reported that, in their investigative work, such patients often had health records requiring several boxes for storage.

Therapeutic responses that are associated with PMDs include the following: unresponsiveness to appropriate medications, response to placebo, and remission with psychotherapy [ 4 ] . An important clue to PMDs is the lack of response to usually effective treatments, such as propranolol for essential tremor or botulinum toxin injections for dystonia. An important proviso is that adequate doses must be achieved in order to state there is lack of response to treatment. Therefore, the physician must be aware of the appropriate trial dose and the expected response, as well as treatment conditions that may modify response before using this as diagnostic criteria. Alternatively, PMDs may show dramatic response to placebo and/or suggestion. This improvement may be transitory, but as this can also occur in organic disorders, it should not form the sole basis for a psychogenic diagnosis [ 10 ] . A confi rma-tory feature is complete remission with psychotherapy [ 4 ] . Patients may also respond to pharmacological treatment (SSRIs, tricyclic antidepressants) or eletroconvulsive therapy when depression and anxiety underlie the PMD [ 22 ] .

The diagnosis of PMD requires a keen investigative mind along with obtaining collateral information in addition to the patient’s history and a prolonged and detailed physical examination and excellent documentation of the consultation. While medicine consists of many exceptions to the rule, including within the presentation of movement disorders, that PMD patients require longer to assess than those with organic illness is a consistent fi nding.

Diagnostic Criteria

Fahn and Williams Diagnostic Criteria

Williams et al. set forth criteria to assist in the clinical diagnosis of PMDs [ 1 ] . The classifi cation scheme allows categorization according to the degree of diagnos-tic certainty as documented, clinically established, probable, and possible. The authors suggested that the categories of documented and clinically established could be combined to form the category of clinically defi nite.

Documented PMD

In order for a PMD to be classifi ed as documented, it “must be persistently relieved by psychotherapy, with or without associated psychotropic medication.” Alternatively, it is suffi cient if symptoms may be seen to spontaneously remit when the patient is unaware of being observed, as seen in malingering or factitious disorder, since these disorders are unlikely to respond to psychotherapy [ 1 ] . Response to hypnosis,


amobarbital, sedatives, or placebo is not suffi cient to establish a psychogenic diagnosis, as organic movement disorders may demonstrate transient improvement with these agents. Spontaneous remission is also insuffi cient to establish a psycho-genic diagnosis, because organic movement disorders, such as tics and ataxia, may have a fl uctuating course.

Clinically Established PMD

A psychogenic etiology for a movement disorder should be strongly suspected in a patient who presents with inconsistent symptoms and signs and also when the presentation of the movement disorder is incongruent with the typical presentation of an organic movement disorder [ 1 ] . Factors supporting this diagnosis consist of other physical psychogenic signs, such as false weakness or sensory loss, multiple somatizations, and an obvious psychiatric diagnosis.

Probable PMD

Three categories of patients fall under the probable PMD classifi cation [ 1 ] . The fi rst category consists of patients who manifest movements that are inconsistent or incongruent with an organic movement disorder, but lack other features to support a diagnosis of PMD. The second category includes patients who manifest abnormal movements that are consistent and congruent with an organic disorder, but also have coexistent psychogenic signs, such as false weakness or sensory loss. The third category is comprised of patients whose movements are consistent and congruent with an organic disorder, but also manifest multiple somatizations.

Possible PMD

This classifi cation includes patients whose movements are 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, until a defi nite organic or psychogenic etiology is confi rmed [ 1 ] . The features that suggest a psychogenic diagnosis include, “inappropriate affect, a discrepancy between the movement disorder and the reported disability, or the presence of secondary gain” [ 1 ] .

Gerber and Shill Diagnostic Criteria

Shill et al. [ 23 ] devised an alternate set of diagnostic criteria, with two categories, clinically probable and clinically possible. Their aim in developing these criteria was to simplify the diagnosis of PMDs, in order to facilitate proper treatment and


avoid unnecessary diagnostic tests and inappropriate treatments. They retrospectively reviewed 29 patients diagnosed with PMDs and 50 patients diagnosed with organic neurological disorders and determined that their criteria had a sensitivity of 83% and a specifi city of 100% in identifying “clinically probable” (or better) PMDs and 97% sensitivity and 96% specifi city in identifying “clinically possible” PMDs.

Clinically Proven PMD

Clinically proven PMDs may be diagnosed when the disorder remits with psycho-therapy and remits when the patient believes they are unobserved or when there is Bereitschafts potential on electroencephalography [ 23 ] . Those patients not meeting the criteria of clinically proven PMD may be classifi ed as either clinically defi nite, clinically probable, or clinically possible. The classifi cation depends upon whether they meet certain diagnostic criteria. Primary diagnostic criteria include the presence of factors inconsistent with organic disease, the presence of excessive fatigue or pain, previous exposure to a disease model, and/or potential for secondary gain. Secondary criteria include multiple somatizations (other than fatigue and pain) and/or apparent psychiatric disturbance.

Patients fulfi lling at least three primary criteria and at least one secondary criteria are classifi ed as clinically defi nite PMD. Patients fulfi lling two primary criteria and two secondary criteria are classifi ed as clinically probable PMD. Clinically possible PMD is defi ned by one primary criterion and one secondary criteria or two primary and one secondary criteria.

The validation of diagnostic criteria for PMDs is limited by the fact that evaluation of PMDs is primarily clinical, with no applicable imaging or pathological fi ndings. Since PMDs are defi ned as the absence of organic illness, they are a diagnosis of exclusion. A thorough history and physical examination are necessary to detect any underlying organic etiology. If there remains any diagnostic uncertainty after the examination, then imaging and/or electrophysiological testing may be appropriate. Multiple assessments may be required, and a trial of medication may be necessary with standardized examination where possible.

Rating Scale for PMDs

Hinson et al. [ 24 ] have developed and validated a rating scale to assess PMDs. The scale consists of three parts. In the fi rst part, each of ten phenomena (rest tremor, action tremor, dystonia, chorea, bradykinesia, myoclonus, tics, athetosis, ballism, and cerebellar incoordination) is rated as present or absent. If present, each is assigned a severity grade and duration factor for each of 14 body regions individually, with scores from 0 (lowest) to 4 (highest). There was good inter-rater reliability for the presence or absence of each phenomenon, with total agreement among three raters for all patients and phenomena in 89%. Next, Global Severity and Global


Incapacitation scores are assigned, with a similar range from 0 to 4, refl ecting the overall severity and incapacity. Part 2 rates the presence, severity, duration, and incapacitation of two functions, gait and speech. In Part 3, the scores are summed, leading to a Total Phenomenology Score, refl ecting the summed ratings of the ten phenomena, and a Total Function Score, refl ecting the summed ratings of the two functions, gait and speech. The Total Psychogenic Movement Disorder Score is the sum of the Total Phenomenology Score and the Total Function Score. A high rate of agreement between raters assessing overall PMD burden, including total phenomenology, function, and total PMD scores, was seen. This indicates that the scale is both reliable and valid, making it a useful tool for the assessment and monitoring of PMD patients.

Clinical Features of PMDs

Tremor

Tremor is defi ned as a rhythmic, sinusoidal oscillation of a body part. Psychogenic tremors may have postural, kinetic, and resting components. Psychogenic tremor may be diagnosed using a modifi ed version of the Fahn criteria for psychogenic dystonia [ 25 ] and was used in a study of 25 patients presenting to a movement disorders clinic for evaluation [ 26 ] . A diagnosis of psychogenic tremor was accepted if other possible causes of symptomatic tremor were excluded (such as medications, thyroid dysfunction, hormonal, and metabolic dysfunction) and if there was no evidence of essential tremor, parkinsonian tremor, or other neurological disorder. Further, there must be a period of at least 2 weeks during the observation period in which no tremor was present. Features of psychogenic tremor include dis-tractibility with complex contralateral tasks or concentration on memory or math-ematical problems, variability of amplitude, distribution, frequency, and direction and entrainment by tests of coordination [ 1, 4, 5 ] . Observation over a prolonged period is often necessary to detect these variations. Observing the tremor in various positions (sitting, hands extended, legs extended, lying down, and walking) is necessary. To state that tremor is present at rest, the patient must be examined lying down with the arms completely rested on the examination table at their sides—not held over their abdomen. With changes in position, the direction of the tremor may change. For example, fl exion-extension tremor of the wrist while sitting becomes side-to-side while lying. Observing the patient with a critical eye to the features of tremor (position or posture that brings it out, frequency, amplitude, direction, and distribution) must occur throughout the examination. Other characteristics of psychogenic tremor are abrupt onset with bilateral involvement and a nonprogres-sive course with fluctuating severity [ 27, 28 ] . Associated disabilities tend to be selective, rather than task specifi c. The neurological examination frequently reveals inconsistencies, such as distractibility and entrainment, demonstrated in the


accompanying video. Distractibility occurs when the tremor halts or changes in frequency and/or amplitude when the patient is asked to perform distracting activities. Entrainment occurs when the tremor frequency changes to match the frequency of the distracting activity in another limb. Suggestibility is common and may result in complete resolution of tremor. Attempting to restrain the shaking limb typically results in marked increase in tremor amplitude and force; in essential or physiologic tremor, the speed and amplitude would dampen.

Accelerometry may be employed to document distractibility, entrainability, and inconsistency of frequency of psychogenic tremor; demonstrate an increase in amplitude or change in frequency in tremor when the limb is loaded with weight; and determine that the tremor lacks a frequency and amplitude characteristic of organic tremor types [ 26– 30 ] . Electromyography may demonstrate co-activation of antag-onist muscles in psychogenic tremor. Thus, psychogenic tremor can be diagnosed positively using neurological signs and should not be considered solely a diagnosis of exclusion [ 27– 29 ] .

Dystonia

Dystonia is syndrome of “involuntary torsional movements with a tendency toward sustained posture at the peak of the movements” [ 1 ] . When first described, dystonia was considered to be a psychiatric disease. The explanation provided by psychiatrists was that patients were turning away from confl ict. By the turn of the century, neurologists recognized an underlying organic causation [ 31, 32 ] . By midcentury, the organic basis of dystonia was again called into question, with many patients having organic dystonia referred for psychiatric treatment [ 32 ] . Many features of psychogenic dystonia and organic dystonia overlap. For instance, both may display variation in speed and quality of movements and may be paroxysmal, stereotyped, and repetitive. Further, organic dystonia may be strikingly task specifi c—recall patients with musician’s dystonia—while a patient with PMD may seek to avoid work. Dystonia characterized by tremor, such as a dystonic neck tremor may display a null point when tremor is completely ablated. Patients may have diffi culty sitting looking straight forward, yet show little deviation while walking. Similarly, while sitting quietly, no involvement may be present, yet when taking up the pen, the wrist may deviate twisting the entire arm around. These last features are suspi-cious for PMD to the uninitiated physician, yet to those familiar with the behavior of dystonia, are quite consistent with organic illness. Another feature of organic dystonia that may have led credence to the belief of “turning their head from confl ict” is the ability to resolve dystonia with a light, nonrestrictive touch to the chin or neck or head. This geste antagonist must surely have caused suspicion among early physicians. While consistency is emphasized as characteristic of organic movement disorders, the exception of dopa-responsive dystonia with its striking diurnal variation again highlights the need for neurologists to constantly revise and update their knowledge of movement disorders.


Features characteristic of psychogenic dystonia include inconsistency, variability, and incongruity with typical presentations of organic dystonia [ 1, 4 ] . Other clues that the dystonia may be psychogenic in nature are sudden or dramatic onset, onset of dystonia in the foot in an adult (unless associated with a parkinsonian state since this is characteristic of parkin carriers) or at rest, and onset of fi xed dystonia, especially appendicular dystonia following trivial peripheral injury [ 33, 34 ] . The accompanying video depicts a key feature that leads to a diagnosis of psychogenic dystonia, namely, the abrupt onset in an adult of a fi xed dystonia in a limb following peripheral injury.

Associated features of psychogenic dystonia may also help to distinguish it from organic dystonia including false weakness, nonorganic sensory changes, and multiple somatizations [ 1, 27 ] . In contrast to organic dystonia, pain is a prominent feature of psychogenic dystonia, which often occurs in conjunction with complex regional pain syndrome [ 33, 34 ] . Medications such as dopamine-blocking agents may induce sudden onset dystonia and remission once the medication is stopped [ 13, 27 ] .

Conventional electromyography cannot differentiate between organic and psycho-genic dystonia since both demonstrate co-contraction of antagonist muscles [ 1 ] . However, organic dystonia is characterized by a reduction in reciprocal inhibition in the H-refl ex by electrical stimulation. A recent study demonstrated that psychogenic dystonia patients may share similar electrophysiological abnormalities with organic dystonia patients, possibly due to the effect of a fi xed posture inducing changes in the central nervous system [ 35 ] . Thus, treatment aimed at psychological abnor-malities alone may be insuffi cient. Therapy that attempts to restore normal physiology such as biofeedback or motor training may be benefi cial in both organic and psy-chogenic dystonia [ 35 ] .

Myoclonus

Myoclonus is a “sudden, brief involuntary movement caused by shock-like muscular contractions” [ 1, 4 ] (Chap. 5 ). Psychogenic myoclonus tends to be distractible, variable in amplitude, frequency, latency, and anatomical distribution, and the phenomenology is incongruous with typical organic myoclonus [ 36 ] . Psychogenic myoclonus is usually segmental in nature, occurs at rest, and is exacerbated by voluntary movement [ 27 ] . It may be triggered by manipulation of a distal part of the body. For instance, in a patient with head bobbing, striking the patellar refl ex may induce myoclonus in the neck and may be provoked with suggestibility. The diagnosis is supported by worsening and relief with placebo and suggestion, spontaneous periods of remission, rapid onset, and sudden resolution with or without suggestion. Psychogenic myoclonus also shows signifi cant habituation with repeated stimulation [ 36 ] .

In organic myoclonus, electromyography will usually show a brief burst of 10–70 ms, whereas psychogenic dystonia will show a latency within the range of


voluntary reaction time (100–120 ms) and a more variable and inconsistent pattern of muscle activation [ 1, 21 ] . Electroencephalography with back averaging from the myoclonic movement typically will show a Bereitschafts potential in psychogenic myoclonus, indicating a voluntary component to the movement. Thus, clinical examination and electrophysiological recordings are helpful in distinguishing psychogenic from organic myoclonus [ 36 ] .

Tics

Tics are “paroxysmal, stereotyped, repetitive movements that can be simple or complex, usually preceded by an inner urge or motor sensation, and followed by a transient sense of relief of inner tension” [ 1 ] (Chap. 4 ). Tics, by their very nature, have a voluntary component. Often, Tourette syndrome patients report a premoni-tory sensory symptom that results in the movement to relieve the symptom. Other features shared by both organic tics and psychogenic tic disorders include suppressibility, waxing and waning course, replacement of one movement or tic with another, and a certain degree of variability. Tics are also worsened with anxiety and stress, and these may also worsen tics in PMD. Further, patients with Tourette syndrome may have echopraxia (repeating a gesture or movement of another person). Perhaps, one clue to PMD tics would be the presence of secondary gain. For many patients with organic tics or Tourette syndrome, the tics bring isolation and embarrassment rather than benefi t.

Chorea/Athetosis

Chorea describes “abrupt, rapid, random, unsustained, purposeless movements that spread from one body part to another” [ 1 ] with athetosis being a more sustained, writhing type of movement. Psychogenic chorea/athetosis may be diffi cult to differentiate from organic etiologies due to the characteristic random anatomical distribution of chorea and the relatively sustained nature of athetosis. Outbreaks of psychogenic chorea or “dancing mania” have been noted in history to occur in a climate of accentuated religious fervor, otherwise known as mass hysteria or epidemic hysteria [ 37, 38 ] .

Perhaps, the most challenging PMDs to diagnose are the paroxysmal chore-oathetotic disorders. These include PMD counterparts of paroxysmal kinesigenic and nonkinesigenic dyskinesias (choreoathetosis) (see Chap. 6 ). In paroxysmal kinesigenic dyskinesias, onset typically is in childhood or early adulthood, and a positive family history is often present with an autosomal dominant pattern of inheritance. Episodes of dyskinesia are brief, lasting seconds. Although patients may have up to 100 a day, there is typically a refractory period after each attack. Many patients have complete remission once adolescence is complete. In paroxysmal


nonkinesigenic dyskinesia, episodes are longer lasting (5 min to hours). Although typically inherited in an autosomal dominant fashion, sporadic cases are seen. Again, onset is in childhood although it may present as late as age 30 years.

Gait Disorders

Disorders of gait are likely to be psychogenic when the phenomenology is not consistent with known organic etiologies and no underlying abnormality can be detected on evaluation of coordination, balance, vision, vestibular function, motor function, and sensory function [ 1 ] . One example is PMD gait that is slow, yet there are no other signs to suggest parkinsonism. Astasia-abasia is the classic hysterical gait, described by Blocq in 1888 [ 1 ] . It is marked by the inability to stand or walk despite normal leg function while seated or lying down. Other described types of psychogenic gait include hemiparetic, slow gait, pseudoataxia, as if walking on ice or a tightrope, and buckling [ 21, 39 ] . These disorders should be distinguished from a cautious gait, characterized by a shorter stride, lower center of mass, widened base, and slower velocity, as an adaptative response to an underlying fear of falling, which may be seen in the elderly [ 40 ] .

Features that suggest a psychogenic gait disturbance include an inability to walk despite normal strength testing while lying down, the need for excessive assistance despite minimal impairment, throwing one’s body at nearby examiners while gait is observed, abrupt fl uctuations in stance, and gait yet, when assistance is not available, remaining upright. Patients are often described as lurching or having exaggerated swaying and moving of the arms. Patients may perform a deep knee bend when asked to perform tandem gait, their arms swooping as if in fl ight, yet never fall. It is striking that such postures are uneconomical in terms of energy requirement. When patients with organic weakness or instability walk, they do so with little fl ourish. PMD patients may also report multiple falls without injury. The presence of bizarre movements of the head, jaw, and arms; a paradoxical ability to walk backward, but not forward (the exception being foot dystonia that improves walking backward, particularly for those with DYT1); excessive slowness or hesi-tation; and gait improvement with distraction should also raise the consideration of PMD [ 40– 43 ] . The accompanying video demonstrates classical astasia-abasia showing abnormal posturing while walking without actually falling such that the ability to avoid falling reveals that the patient actually has excellent strength, coor-dination, position sensation, and postural refl exes.

Patients with psychogenic gait may respond with rapid resolution in response to placebo, psychiatric intervention, or simple identifi cation of the gait as psycho-genic. A multidisciplinary approach with enlistment of the family and physiothera-pist for “gait retraining” is especially helpful. Prognosis is poor for patients with persistence of gait dysfunction for a year or more, as many of these patients are diagnosed with a major underlying psychiatric disorder; over 50% will show no improvement in their psychogenic gait over time [ 40 ] .


Exaggerated Startle Refl ex

Exaggerated startle, termed hyperekplexia, is a characteristic of both psychiatric conditions and pathological startle disease, an organic familial disorder caused by a mutation in the glycine receptor (GLRA1) [ 1 ] (Chap. 5 ). Physiologic startle is generated within the nucleus pontis caudalis of the brainstem reticular formation in the fi rst phase and then more broadly based including both the amygdala and other cortical and brainstem structures. In normal individuals, complex startle behavior may include vocalization and motor behavior. Psychogenic exaggerated startle tends to be variable, inconsistent and may lead to prolonged postures or an attack of complex abnormal movement. In some cultures, exaggerated startle is common in response to trivial stimulus (Latah, Myriachit, and the Jumping Frenchmen of Maine), and many authors consider these movements to be culturally determined and learned.

Electrophysiology of psychogenic startle shows latency of onset from the stimulus to be similar to voluntary movements and have a triphasic pattern of agonist–antagonist–agonist muscle activation. If startle is similar to stimulus-induced myoclonus, the electrophysiology will show latency of onset to movement between 40 and 100 ms [ 1 ] .

Functional Weakness and Sensory Loss

As functional weakness and/or numbness may coexist with PMDs, a brief descrip-tion of both is presented here. Functional weakness and sensory loss typically do not present in an anatomic distribution [ 44 ] . Rather, functional weakness tends to present with weakness of an entire limb, paraparesis, or hemiparesis [ 44 ] . Functional weakness resembling an upper motor neuron lesion does not demon-strate appropriate change in tone, with spasticity, clonus, hyperrefl exia, or an extensor plantar response. The functional lower motor neuron lesion does not respect normal or variations in normal innervation of a single nerve root or nerve with associated appropriate sensory changes. Similarly, functional sensory loss tends to present with loss of all sensory modalities in an entire limb or in a hemisen-sory distribution [ 44 ] .

Techniques useful in diagnosing functional weakness include observation of limb movements in sleep, the arm drop test (suspending the plegic arm over the supine patient’s face then abruptly allowing it to fall, taking care to shield the face—in nonorganic weakness, the patient will deflect the arm from hitting the face), and the Hoover’s test (observation of weak downward force in the con-tralateral leg when a supine patient is asked to lift either the plegic leg or the normal leg may indicate functional weakness) [ 44 ] .

Functional sensory loss may be detected using various techniques including the yes–no test. Patients are asked to say “yes” when they detect a stimulus and “no”


when they do not detect a stimulus; a response of “no” immediately after a stimulus may indicate nonorganic sensory loss—while the truly anesthetic patient does not feel anything, and so, would not say no. Another test is the Bowlus–Currier test where the patient’s own fi ngers are interdigitated with the arms in a twisted posture, making it diffi cult for the patient with functional sensory loss to respond consistently and correctly to alternating stimulus. The Forced-Choice test where patients are asked to distinguish between either a sharp or dull stimulus or upward or downward movement of a toe/fi nger, a percentage of correct responses in a series of trial that is less than that observed by chance, may indicate nonorganic sensory loss [ 44 ] .

It should be remembered that no diagnostic technique is completely reliable; rather, they may be employed in the context of overall evaluation of the patient, taking into consideration other factors that accompany PMDs. PMDs may defy neat classifi cation because they are not limited by the constraints applying to organic movement disorders. Thus, they may present with incongruous combinations of different movement types and novel, bizarre movement types. The entire patient presentation must be considered to make the diagnosis of PMD as outlined in the preceding diagnostic criteria.

Treatment and Prognosis

It is important to fi rst complete a thorough history and physical examination and any further testing deemed necessary to rule out an organic etiology, such as imaging or electrophysiology. The art of this diagnosis is to perform suffi cient tests to rule out likely organic illness but not investigate so extensively that the sick role is reinforced or that new possible etiologies emerge from tests with subjective interpretation. PMD is a neurological diagnosis made by a neurologist. Absence of obvious psychological stress or other contributing factors cannot be determined in a single psychiatric assessment and should not be used to rule out PMD. Once it has been determined that the movement disorder is likely psychogenic in nature, then a diag-nosis can be delivered. This is a crucial step in the process, and the approach taken will set the stage for a therapeutic physician–patient relationship [ 4, 10 ] .

The patient should be told the type of movement disorder that they are manifesting, i.e., tremor, and instructed that the underlying cause is not a severe or permanent structural brain disease, but rather, their illness is due to a complex interaction between the mind and body. They should be reassured that their symptoms may respond to treatment of underlying contributing factors, such as stressors and psychological issues. It may be helpful to compare the situation to other types of illnesses linked to psychological factors, such as peptic ulcer disease, which may be linked to stress [ 4, 16 ] .

PMD patients should be referred to a psychiatrist with an interest in patients with neurological or other medical disorders, and preferably PMDs, to assist with identifi cation and treatment of underlying psychopathology. Somatoform disorders


may respond to treatment, but are subject to relapse [ 1, 18, 22 ] . Patients with somatoform disorder, who refuse psychotherapy, have a poor prognosis, and spontaneous remission is uncommon.

Studies have shown persistence of PMD symptoms in 65–95% of patients [ 10, 18 ] . A study of 42 patients diagnosed with hyperkinetic PMD found that 90% had persistence of abnormal movements and psychopathology after an average of 3.2 years follow-up [ 19 ] . Also, 38% of this group of patients developed additional unexplained medical symptoms during follow-up. A better prognosis is encountered in patients diagnosed with conversion disorder, who are younger than 40, have had a short duration of symptoms, and a recent change in marital status. An underlying diagnosis of depression or anxiety also leads to a more favorable prognosis [ 18 ] .

Prognosis is poor for PMDs associated with long-standing symptoms, insidious onset of symptoms, psychiatric diagnosis of personality disorder, hypochondriasis, factitious disorder or malingering, and the presence of secondary gain [ 10, 18, 45 ] . Resistance to the psychogenic diagnosis and lack of willingness to participate in psychiatric treatment are other factors leading to poor prognosis for recovery [ 4, 10 ] .

Factitious disorders are resistant to treatment. Malingering is by defi nition not amenable to psychiatric treatment, but may remit when the goal is attained or deemed out of reach or the patient is confronted, often in the setting of a lawyer’s offi ce or the courtroom, with obvious evidence of their deception [ 1, 4, 22 ] .

Psychotherapy is a mainstay of treatment of PMDs, and uncovering the underlying psychological factors may be key in promoting improvement of the disorder [ 18, 22 ] . A recent study found that cognitive behavioral therapy, including stress management, activity regulation, emotional awareness, cognitive restructuring, and interpersonal communication, was signifi cantly more effective in the treatment of somatization disorder, compared to a standard treatment regimen of medical care with psychiatric consultation [ 46 ] . Another study found signifi cant improvement in Psychogenic Movement Disorder Rating Scale scores, depression and anxiety scores, and Global Assessment of Function in PMD patients with conversion disor-der treated with psychotherapy [ 47 ] . A meta-analysis showed that 71% of patients with somatization syndromes showed a defi nite or possible treatment effect of cognitive behavioral therapy [ 10 ] . It is interesting to note that the commonest use of cognitive behavioral therapy, outside of somatization disorders, is anxiety and obsessive–compulsive disorder.

Pharmacological treatment may be helpful when an underlying psychiatric condition is present. Specifi cally, depression or anxiety responds well to pharmaco-therapy with many well-tolerated agents available [ 10, 18, 22 ] . An open-label study of antidepressant treatment noted marked improvement in both motor and global outcomes as assessed by Clinical Global Impressions—Severity of Illness scale in 8 of 10 patients with conversion disorder and a history of comorbid depression or anxiety, with remission occurring in 7 of the 10 [ 20 ] . Patients with associated borderline personality disorder also improve with treatment of depression and anxiety. In 5 patients with primary hypochondriasis, somatization disorder, or prob-ably factitious disorder/malingering, there was no improvement [ 20 ] .

Stress management and relaxation techniques may prove benefi cial [ 10 ] . Hypnosis was shown to be as effective as psychotherapy in one randomized controlled trial [ 49 ] .


Referral for physical and occupational therapy may also be helpful to improve motor function when the therapist is enlisted in the whole therapeutic approach and encourages independence rather than the sick role in the patient [ 18, 22 ] .

Intensive inpatient treatment has been advocated in some cases, including the use of placebo administration. However, this may not be practical in today’s complex economical and legal environment surrounding the practice of medicine [ 18, 22 ] . Further, the ethics of placebo administration are clear—patients must be aware that the placebo is a possible treatment, and multiple trials with observation need to occur with both patient and physician blinded to treatment assignment in order to obtain accurate reporting. Hospitalization typically involves a multidis-ciplinary approach with the participation of a movement disorder neurologist, psychiatrist, and therapists and includes medications, psychotherapy, hypnosis, and biofeedback, occurring over many weeks or months [ 48 ] . Psychiatric hospitalization may be required in extreme cases, when the patient is at risk for self-harm, such as in Munchausen’s syndrome [ 18, 20 ] . As a practical note, many insurers will provide benefi ts and healthcare coverage to those diagnosed with a somatoform disorder, while the term “psychogenic movement disorder” may not be viewed equivalently to the insurance carrier.

A retrospective review of a series of 24 patients treated with an integrated multidisciplinary approach noted complete remission in 25% of patients, consider-able improvement in 21%, and moderate improvement in 8% at the end of active treatment [ 1 ] . The study found substantial improvement was sustained for longer than 1 year in 54% of PMD patients. However, some relapse of initial improvement was noted in 20% of patients at follow-up.

There are currently no guidelines for the treatment of PMDs. However, a recent round-table discussion of leading experts in PMD produced a set of treatment strategies [ 50 ] . The consensus was that a psychiatrist should evaluate the patient for underlying psychopathologies, including primary and secondary psychiatric diagnoses, and, in association with other treating physicians, develop a treatment plan that may include psychotherapy (cognitive behavioral therapy or psychody-namic psychotherapy) and pharmacological therapy for comorbid depression and anxiety [ 50 ] . Psychotherapy should focus on underlying factors associated with the PMD such as personality, psychiatric disorders, psychosocial experiences, and behaviors that reinforce and perpetuate the PMD. The patient may also benefi t from stress management techniques, including yoga, meditation, and biofeedback. The patient may be referred for rehabilitation, including physical therapy and occupa-tional therapy. Referral to other specialists may be benefi cial to the extent needed to rule out potential underlying organic disorders [ 50 ] .

Conclusion

In summary, diagnosing PMDs requires an extensive knowledge of organic movement disorders, including their typical and variant presentations; a detailed history, often seeking other information sources, such as family and friends; and careful examination.


Early diagnosis and intervention is essential to optimizing the outcome. Partnership with a psychiatrist, physiotherapist, and occupational therapist interested in such patients is crucial in the successful treatment of PMDs. For movement disorders neurologists, PMDs remain the most challenging diagnoses to establish and treat. Their resistance to treatment results in signifi cant morbidity with substantial economic impact on healthcare expenditures, lost productivity, and psychological distress both to the patient and their families. Improved recognition and a comprehen-sive approach to treatment offers the best hope for “cure” as well as timely access to accurate identifi cation.

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