Chapter 25 Psychogenic movement disorders
Phenomenology, diagnosis, and treatment
Introduction
An entire international symposium on psychogenic movement disorders was held in late 2004, and the subsequent publication of its proceedings is now available (Hallett et al., 2006). That volume covers all aspects of psychogenic movement disorders, beyond the scope of this chapter, and scholars in the field are encouraged to read it. A second symposium was held in April 2009, and its proceedings will be published soon.
Psychogenic movement disorders are caused by psychological factors rather than by an organic etiology. Other terms such as functional, nonorganic, and medically unexplained symptoms have been used. Although the term functional might be more convenient to convey to patients and their families – because of old stigmas regarding having a psychological disorder – the term psychogenic describes the condition best because it refers to the etiology. This is much the same way neurologists label many disorders, such as postencephalitic parkinsonism, vascular parkinsonism, post-traumatic parkinsonism or drug-induced parkinsonism. Why not label parkinsonism due to psychogenic etiology as psychogenic parkinsonism? It places the emphasis on etiology and thereby guides the physician towards appropriate treatment. The term functional has been used in the past to denote organic diseases in which a specific cause was not determined, and has been applied to organic illnesses such as chorea, epilepsy, and neuralgias because these were considered physiologic, rather than anatomic, disorders (see historical reviews by Fahn, 2006a; Munts and Koehler, 2010). Today, for most clinicians, the meaning of functional is synonymous with psychogenic, but this might not be uniformly defined this way, so it would be less ambiguous to use psychogenic. The term organic is used to mean “not due to a psychogenic etiology,” and, thus, the term nonorganic refers to psychogenic. More and more the literature in neurology has adopted the term psychogenic, as can be seen by the epilepsy specialty. The terminology debate in epilepsy appears to be not about psychogenic terminology, but about whether the episodes should be called psychogenic nonepileptiform seizures or attacks (Benbadis, 2010; LaFrance, 2010).
Frequency
Psychogenic disorders in neurology have been estimated to occur in 1–9% of all neurologic diagnoses (Marsden, 1986; Lempert et al., 1990). Neurologists usually and appropriately recognize patients with psychogenic movement disorders, but the patients often do not accept this diagnosis and seek other opinions, going from physician to physician, seeking a diagnosis that is more to their liking. Therefore, a strategy is necessary for the best way to inform the patients of the diagnosis. This issue is discussed in this chapter. Another common situation is that many physicians do not offer the time-consuming care that is necessary to restore such patients to normality, preferring instead merely to diagnose the condition and have the referring physician deal with the healing.
Like other subspecialties in neurology, psychogenic movement disorders are not uncommon. In one large movement disorder clinic, such patients account for 10% of all non-parkinsonian new patient visits (Portera-Cailliau et al., 2006). Typically, patients are diagnosed by the predominant movement feature, e.g., psychogenic tremor, psychogenic dystonia, psychogenic myoclonus, etc. When evaluated this way, tremor is the most common psychogenic phenomenology, followed by dystonia.
Importance of an accurate diagnosis
The diagnosis of a psychogenic movement disorder is a two-stage process (Lang, 2006). First is to make a positive diagnosis that the movements are psychogenic and not due to an organic illness. Second is to identify a psychiatric disorder or the psychodynamics that could explain the etiology of the abnormal movements and prepare the way to deciding the best course for therapy of the individual patient. Deciding between abnormal movements due to a psychogenic cause and an organic one can be extremely difficult. Never having seen strange movements before and pronouncing them to be psychogenic therefore is not a satisfactory method because not even senior movement disorder specialists have seen the whole gamut of organic abnormal movements. An organic cause of the movements needs to be excluded (Fahn, 1994; Williams et al., 2005). But this alone is insufficient and neurologists in times past and present advise that making a diagnosis of a psychogenic disorder depends on finding positive criteria and not simply failing to finding an organic cause (for historical review, see Fahn 2006a).
If the obverse occurs – that is, if a patient is given a diagnosis of a psychogenic movement disorder when, in fact, he or she suffers from an organic one – again the wrong treatment is given. In this situation, time-consuming and expensive psychotherapy, psychiatric medications, and possibly electroconvulsive therapy might be initiated instead of more appropriate pharmacotherapeutic agents that could provide relief. Moreover, a diagnosis of a psychogenic disorder can create emotional trauma for the patient and his or her family (Cooper, 1976). It is important to point out that no matter how much experience a clinician has had, encountering a new type of movement disorder for the first time does not automatically make this a psychogenic movement disorder. For example, task-specific jaw tremor (Miles et al., 1997) is rare, and even when it is encountered for the first time, a wise clinician should consider it to be organic (Video 25.1) and not psychogenic (Video 25.2). 
Neurologic symptoms and signs are a common result of hysteria, and neurologists have long been fascinated by the brain’s ability to be able to produce such clinical expressions on the basis of psychological disturbances. Many great neurologists, such as Charcot and Freud, intensively studied hysterical conversion reactions, using hypnosis as a tool in their investigations and treatment (Goetz, 1987). In their training, neurologists-to-be are taught to differentiate the clinical findings of psychogenic etiology from those of organic disorders (Gowers, 1893; Oppenheim, 1911a; DeJong, 1958a). However, textbooks in the past often considered some dyskinesias, recognized today as organic, such as tics, writer’s cramp and other occupational cramps, and some other forms of dystonia, to be examples of hysteria (DeJong, 1958b).
Although there is a modest neurologic literature on psychogenic phenomenology, the literature dealing specifically with psychogenic movement disorders is rather sparse. For example, tremor as the result of a conversion reaction has been long recognized, at least since the days of Gowers (1893), but scientific reports on psychogenic tremor or other movement disorders are rarely described in the literature. Campbell (1979) pointed out that the amplitude of psychogenic tremor is more pronounced when attention is paid to it, and that it lessens and may even disappear when the patient’s attention is diverted to another subject or other part of the body. Distraction is a useful part of the examination, and lessening of severity by distraction can be very helpful diagnostically in trying to establish a diagnosis of psychogenic tremor. But in our experience, distraction does not always succeed in making the tremor disappear, so this maneuver is often not successful. Therefore, additional findings on examination are often necessary and can be just as helpful in considering the diagnosis of a psychogenic movement disorder; these are discussed in this chapter.
Although in the great majority of patients with a psychogenic movement disorder, all their clinical features result only from a psychogenic problem, some may have the psychogenic movement disorder on top of an organic movement disorder, as seen in Patient 5 in the series of psychogenic dystonias reported by Fahn and Williams (1988) and the cases of Ranawaya and colleagues (1990). Perhaps 10–15% of patients with a psychogenic movement disorder have an underlying organic movement disorder as well. This overlap is seen in patients with psychogenic seizures (“pseudoseizures”); 10–37% of patients have organic seizures as well (Krumholz and Niedermeyer, 1983; Lesser et al., 1983). Nevertheless, a useful rule of thumb is that if one part of the examination reveals nonorganicity, it is likely that other “abnormalities” on the examination might also be nonorganic.
Perhaps the movement disorders with the highest prevalence rate of a psychogenic origin are the nonfamilial, “idiopathic”, paroxysmal nonkinesigenic dyskinesias, as surveyed by Bressman and colleagues (1988). They found that of 18 patients with paroxysmal nonkinesigenic dystonias and with no known symptomatic etiology or positive family history for a paroxysmal dyskinesia, the dystonias were due to psychogenic causes in 11 patients. This represents 61% of such cases. The age at onset in these patients ranged from 11 to 49 years; 8 of the 11 patients were female. Thus, unless accompanied by a clear-cut family history, these paroxysmal dystonias are commonly psychogenic, and their diagnosis is extremely difficult to make for reasons that are explained later in the chapter (Fahn and Williams, 1988).
Kotagal and colleagues (2002) conducted a study of paroxysmal events in children. Over a 6-year period, 883 patients were monitored in their pediatric epilepsy monitoring unit; 134 patients (15.2%) were documented to have paroxysmal nonepileptic events. Children in the preschool group (age: 2 months to 5 years) (n = 26) were eventually diagnosed with stereotypies, hypnic jerks, parasomnias, and Sandifer syndrome. The school-age group (age: 5–12 years) (n = 61) had diagnoses of psychogenic seizures, inattention or daydreaming, stereotypies, hypnic jerks, and paroxysmal dyskinesias. The adolescent group (age: 12–18 years) (n = 48) had a diagnosis of psychogenic seizures in 40 patients (83%). The authors concluded that in patients with paroxysmal nonepileptic events, conversion disorder was seen in children older than 5 years of age, and its frequency increased with age, becoming the most common type of paroxysmal nonepileptic events among adolescents. In adolescents, conversion disorder was more common in females, whereas males predominated in the school-age group. Concomitant epilepsy with nonepileptic events occurred in all three age groups to a varying extent.
Mass hysteria
Today, neurologists encounter individual patients with psychogenic movement disorders. But historically, mass hysteria was common, probably more so than it is today. Mass hysteria still occurs, such as “shell shock” in wartime, as well as during current environmental events such as mass inoculations (Kharabsheh et al., 2001; Khiem et al., 2003). Symptoms can also be generated from mass concerns about medications and breast implants, in part owing to widespread publicity, although legal liability issues may also drive the development of symptoms. Mass hysteria resembling seizures occurred recently in 10 high school girls following the development of organic absence seizures in another student (Roach and Langley, 2004).
It is interesting to note on a historical level that the term chorea, meaning dancing in Latin, comes from the dancing mania (a mass hysteria) that was seen in the Middle Ages, and from which the term St Vitus’ dance was coined; this term subsequently was applied by Sydenham to describe the condition now referred to as Sydenham chorea (Hayden, 1981).
For further information, see the 2001 monograph by Halligan and colleagues, which is devoted to the topic of hysteria.
Physiologic basis for psychogenic neurologic dysfunctions – neuroimaging
It is intellectually intriguing that the brain can create neurologic deficits – such as paralysis, sensory loss, blindness, seizures, and movement disorders – from psychological factors. This mysterious ability fascinated pioneers working on hysteria, such as Charcot and Freud. We have not been much enlightened over the ensuing 100-plus years until recently, when newer imaging technologies have shed some light on the mechanism. As stated by Hallett (2010), physiologically, we cannot tell the difference between voluntary and involuntary. The exceptions are electrophysiologic measurements of myoclonus, startle, tremor and blepharospasm. The fast 50–100 ms contractions of organic myoclonus cannot be duplicated by psychogenic myoclonus. Psychogenic startle responses are too delayed and variable to be a physiologic reflex (Thompson et al., 1992). Psychogenic tremor can often be detected by variable width on spiral analysis (Hsu et al., 2009) and by other tests like coactivation sign and tapping (Deuschl et al., 1998, 2006; Zeuner et al., 2003; Criswell et al., 2010). The R2 recovery in the blink reflex is disinhibited in organic blepharospasm and is normal in psychogenic blepharospasm (Schwingenschuh et al., 2011). The Bereitschaftspotential (BP) (readiness potential) is seen with ordinarily voluntary movements, but by itself does not indicate that a movement is voluntary (Hallett, 2010). The electrophysiology of psychogenic dystonia resembles that of organic dystonia (Espay et al., 2006; Quartarone et al., 2009), except for findings of increased plasticity in the latter.
Vuilleumier and colleagues (2001) utilized single photon emission computed tomography (SPECT) to measure regional cerebral blood flow with and without bilateral vibration in seven patients with unilateral psychogenic sensory loss and then again in four subjects after full recovery. These studies revealed a consistent decrease of regional cerebral blood flow in the thalamus and basal ganglia contralateral to the deficit, which reverted to normal when the patients recovered. These results suggest that hysterical conversion deficits might entail a functional disorder in striatothalamocortical circuits controlling sensorimotor function and voluntary motor behavior. The same subcortical premotor circuits are involved in unilateral motor neglect after organic neurologic damage.
In an analogous situation, a patient who was diagnosed with psychogenic reduced visual acuity underwent a SPECT scan that revealed reduced regional cerebral blood flow in the bilateral visual association areas but not in the primary visual areas (Okuyama et al., 2002). The authors concluded that psychogenic visual disturbance is associated with functional suppression of the visual association area. A listing of functional imaging studies carried out in hysteria has been collated by Fink and colleagues (2006). These studies indicate that alterations in regional brain activity may accompany the expression of conversion symptoms. Since then, another study utilizing positron emission tomography (PET) in patients with hysterical anesthesia showed lack of response in the contralateral cortex to sensory stimulation of the affected limb, again indicating the brain physiologically shuts down as a result of the hysterical anesthesia (Ghaffar et al., 2006). Yet when bilateral stimulation is applied, there is bilateral activation of the cortex, indicating that the cortex is indeed intact.
The results in functional imaging studies are complemented by motor physiology studies. When cortical and spinal inhibition was evaluated in psychogenic and organic dystonia, both groups had similar results of reduced inhibition (Espay et al., 2006). Again, this suggests that the central nervous system accommodates its physiology to follow the motor pattern, or the reverse, i.e., that the abnormal psychological problem alters brain physiology, which then produces the abnormal motoric effect.
Degree of certainty of the diagnosis of a psychogenic movement disorder
Fahn and Williams (1988) categorized patients into four levels of certainty as to the likelihood of their having psychogenic dystonia; these categories can be applied to all psychogenic movement disorders. These four degrees of certainty are: (1) documented psychogenic disorder, (2) clinically established psychogenic disorder, (3) probable psychogenic disorder, and (4) possible psychogenic movement disorder. Subsequent authors have used this classification (Koller et al., 1989; Ranawaya et al., 1990; Lang, 1995; Shill and Gerber, 2006). We have incorporated the classification of Fahn and Williams but have expanded the criteria somewhat, taking into account additional observations since the original publication.
Documented psychogenic movement disorder
Just being suspicious that the signs and symptoms are psychogenic is insufficient for the diagnosis of documented psychogenic disorder. For the disorder to be documented as being psychogenic, the symptoms must be completely relieved by psychotherapy, by the clinician utilizing psychological suggestion including physiotherapy, or by administration of placebos (again with suggestion being a part of this approach), or the patient must be witnessed as being free of symptoms when left alone, supposedly unobserved. This last feature would be a major factor in proving psychogenicity in those who are malingering or have a factitious disorder, since such patients would not likely obtain relief of symptoms by manipulation of the examiner. Insurance companies are increasingly using videotaped surveillance to protect themselves against fraud. There is now a published report of a patient with a clinical diagnosis of reflex sympathetic dystrophy who sued for financial compensation despite features of psychogenicity and was videotaped while under surveillance by a private investigator to be completely free of the abnormal movements, allowing the case to be settled for a reduced amount (Kurlan et al., 1997). If the signs and symptoms disappear and do not return, that is fairly good evidence that the underlying psychiatric problem has been relieved. But it is not uncommon for the psychogenic movement disorder to return if the patient does not obtain complete relief of the psychiatric factors that led to the neurologic dysfunction.
A critical issue for using the relief of signs as a criterion for the definition is that most organic movement disorders rarely remit spontaneously and completely except for tics, tardive dyskinesia, infectious (e.g., Sydenham chorea), and drug-induced reactions, and rarely, essential myoclonus (Fahn and Sjaastad, 1991). Other organic disorders, such as Parkinson disease, Huntington disease, and essential tremor, are persistent and even progressive. Idiopathic torsion dystonia, except for torticollis (Jayne et al., 1984; Friedman and Fahn, 1986; Jahanshahi et al., 1990), rarely totally remits. On occasion, patients with other types of dystonia will show improvement, but this improvement is typically incomplete and temporary (Marsden and Harrison, 1974), although gradual, prolonged, incomplete improvement has been encountered in at least one patient (Eldridge et al., 1984).
Clinically established psychogenic movement disorder
When the movement disorder is inconsistent over time (the features are different when the patient is observed at subsequent examinations) or is incongruent with a classic movement disorder, one becomes suspicious that the movements are psychogenic. If either inconsistency or incongruity is present and, in addition the patient has any of the manifestations listed in Table 25.1, one can feel comfortable in believing that the disorder is psychogenic, and this has been referred to as clinically established psychogenic movement disorder.
Table 25.1 Additional manifestations besides inconsistency and incongruity for the diagnosis of clinically established psychogenic movement disorder
It should be noted that item 4 in Table 25.1 by itself is insufficient for a diagnosis of a documented or clinically established psychogenic disorder. This is because some organic movement disorders can be temporarily and voluntarily suppressed (Koller and Biary, 1989). Similarly, akathitic movements and paradoxical dystonia (Fahn, 1989) also tend to disappear with active voluntary movement. The difficulty establishing psychogenic paroxysmal dyskinesias which have a normal interictal pattern is covered below. Fortunately, myoclonus has such a short-duration contraction that it cannot be purposely produced, so electrophysiologic evidence against organic myoclonus could be one of the factors along with inconsistency and incongruity that can lead to a clinically established diagnosis of a psychogenic myoclonus. Psychogenic tremors have features such as a coactivation sign (Deuschl et al., 1998, 2006) or a change in tremor frequency due to entrainment by tapping the contralateral limb (Zeuner et al., 2003). These features would establish the tremor as psychogenic.
Probable psychogenic movement disorder
This definition contains four categories of patients:
Definitions of psychiatric terminology
Somatoform disorder
The abnormal movements of somatoform disorders are involuntary. The knowledge that one is the cause of one’s own actions is known as self-agency. Thus, people with abnormal movements due to a somatoform disorder lack self-agency. The right inferior parietal cortex is the brain area believed to play a role in self-agency. Voon and her colleagues (2010) utilized functional magnetic resonance imaging in eight subjects with a conversion disorder (tremor). The right temporoparietal junction was found to be hypoactive compared to those purposefully mimicking the same type of tremor (P < 0.05). There was an associated reduced connectivity between this cortical area and the sensorimotor areas and the limbic system.
Clues suggesting the presence of a psychogenic movement disorder
Often, there are clues from the history and neurologic examination that lead the clinician to suspect a diagnosis of psychogenic dystonia. Fahn and Williams (1988), Koller and colleagues (1989), and Factor and colleagues (1995) have enunciated many of these clues. Tables 25.2 and 25.3 list these clues, as well as some additional ones.
Table 25.2 Clues relating to the movements that suggest a psychogenic movement disorder
Table 25.3 Clues relating to other medical observations that suggest a psychogenic movement disorder
Abrupt onset of the movement disorder is quite common. The presence of more than one type of dyskinesia (item 5 in Table 25.2) is another important clue, often confounding clinicians (Video 25.3). Most of the time, patients with an organic movement disorder present with only a single type. A note of caution is warranted, however. Certain disorders progress to involve more than one type of abnormal movement. For example, Huntington disease can have chorea, bradykinesia, dystonia, and myoclonus (Penney et al., 1990). Neuroacanthocytosis often is manifested by both chorea and tics (Hardie et al., 1991). Some patients with childhood-onset tics may later develop torsion dystonia (Shale et al., 1986; Stone and Jankovic, 1991). Often, patients with idiopathic torsion dystonia will have dystonic tremor or rapid movements that resemble myoclonus or chorea (Fahn et al., 1987). Patients with tardive dyskinesia may have a combination of rhythmical oral-buccal-lingual movements plus dystonia and akathitic movements (Fahn, 1984). Table 1.17 in Chapter 1 lists the diseases that are composed of multiple types of movement disorders. 
The most common types of movements, whether isolated or in the presence of other types of movements, in patients with psychogenic movement disorders are shaking movements (item 4 in Table 25.2) that can resemble organic tremors or peculiar, atypical tremors (Video 25.4). This was the most common type of abnormal movement in the spectrum of psychogenic movement disorders reported by Lang (2006) and by Jankovic et al. (2006b). Another note of caution about unusual tremors is that Wilson disease can also present with unusual tremors (Shale et al., 1987, 1988). Utterances of gibberish can be another useful sign (Videos 25.5 and 25.6). 
Item 4 in Table 25.2 also lists bizarre gaits as a feature of psychogenicity. After tremors and dystonia, bizarre gait disorders are the next most common type of unusual movement disorder encountered in patients with mixed features of movements. The psychogenic gait can show posturing, excessive slowness, and hesitation. There could be pseudo-ataxia or careful walking (like walking on ice). The latter resembles the fear-of-falling syndrome, which is discussed in more detail later. There can be sudden buckling of a leg, as if there is weakness (Vecht et al., 1991), but the failure to produce this dipping movement each time the patient steps on the leg would be evidence of inconsistency. Accompanying this bizarre gait would be a variability of impairment and excessive swaying when tested for the Romberg sign, without actually falling.
Another aspect of item 4 is excessive startle that could mimic hyperekplexia, excessive startle syndrome, the jumping Frenchmen syndrome (Video 25.7), or even reflex myoclonus (Andermann and Andermann, 1986). Thompson and colleagues (1992) determined the physiologic parameters that are typically seen in patients with psychogenic startles. There is a variable latency to the onset of the jerk; the latencies are greater than those seen in reflex myoclonus of cortical or brainstem origin; the latencies are longer than the fastest voluntary reaction time; there are variable patterns of muscle recruitment within each jerk; and there is significant habituation with repeated stimulation. This last point is probably not specific to psychogenic startle, since organic startles may also show habituation. Noise stimuli can induce other abnormal movements besides startle. Walters and Hening (1992) reported a case with psychogenic tremor following sudden, loud noise; the patient had a post-traumatic stress disorder. 
Item 11 in Table 25.2 points out that in a patient with psychogenic tremor, when asked to carry out rapid successive movements, such as tapping the index finger on the thumb, the rate of the tremor becomes the same as the rapid successive movements (i.e., the tremor has become entrained). In contrast, an organic tremor is the dominant rate; it will gradually force the voluntary movements to be the same rate as the tremor.
Idiopathic torsion dystonia usually begins with action dystonia (Fahn et al., 1987), but psychogenic dystonia often begins with a fixed posture. Fixed postures are sustained postures that resist passive movement, and the presence of such fixed postures is highly likely to be due to a psychogenic dystonia (Fahn and Williams, 1988; Lang and Fahn, 1990; Schrag et al., 2004; Schrag, 2006). The posture can manifest so much rigidity that it is extremely difficult to move the limb about a joint (Video 25.8). Often, the psychogenic dystonia resembles reflex sympathetic dystrophy (complex regional pain syndrome, CRPS) because there is accompanying pain, tenderness (allodynia), and skin changes (Lang and Fahn, 1990; Schwartzman and Kerrigan, 1990; Bhatia et al., 1993; Schrag et al., 2004; Schrag, 2006). Nerve injury leading to pain, shiny red skin, and fixed postures was called causalgia by Mitchell et al. (1864). Charcot (1892) considered the disorder hysterical (see Munts and Koehler, 2010). The term “reflex sympathetic dystrophy” was coined by Evans (1946) because the phenotype could occur in the absence of trauma to a major nerve and might be due to sympathetic nerves. “Complex regional pain syndrome” was the recommended term in 1994, with type 1 being reflex sympathetic dystrophy and type 2 being causalgia (Merskey and Bogduk, 1994). 
To make matters confusing, in many cases, psychogenic dystonia of a limb follows a minor trauma to that limb, similar to the pattern of reflex sympathetic dystrophy. On the other hand, organic dystonia of a body part can be preceded by an injury to that body part (Schott, 1985, 1986; Scherokman et al., 1986; Gordon et al., 1990; Goldman and Ahlskog, 1993), so it can be difficult to distinguish between organic and psychogenic dystonia. Fixed painful postural torticollis following trauma is not uncommon, and determining whether it is organic or psychogenic is difficult, but analysis indicates that many of these cases appear to be psychogenic in etiology (Sa et al., 2003).
Although a fixed dystonic posture, in which the joint cannot be passively extended or flexed, is often psychogenic, it could also be due to a contracture (which, of course could also be the result of a psychogenic dystonia as well as an organic dystonia). The evaluation of such fixed postures in which the affected joint cannot be passively altered requires the aid of anesthesia to see if contractures are present (Fahn, 2006b). This technique not only aids the diagnosis but also guides the clinician and patient in what to expect during therapy (Video 25.9). The prognosis of fixed dystonia is often poor (Ibrahim et al., 2009), but it depends on recognizing this disorder as likely to be a psychogenic one and then applying treatment according the principles described below. 
Debates continue as to whether CRPS is organic or psychogenic. This topic was discussed at the Second Psychogenic Movement Disorder Symposium in 2009. A recent proposal that small fiber neuropathy might be responsible (Oaklander and Fields, 2009) has been countered by the observation that the patient had the phenomenology of a psychogenic dystonia (Lang and Chen, 2010).
In addition to the clues in the history and examination related to the movements themselves presented in Table 25.2, there are often clues in the non-movement history and examination that help the clinician consider a psychogenic disorder. These are presented in Table 25.3.
We have been impressed by the frequency with which patients with psychogenic movement disorders are employed in some capacity working in the health profession (item 6 in Table 25.3). Many are nurses; another large group are employed in the health insurance industry, processing medical claims.
Another point that is worth commenting on is that many of the affected individuals have a devoted spouse who responds readily to their pressing needs (item 7 in Table 25.3). Some spouses carry a pager so that the patient can easily call them while they are at work. Others pamper the patient, who might even be wheelchair bound, especially if the patient has psychogenic dystonia. Such devotion could be a secondary gain from having the movement disorder.
Diagnostic approach and clinical features
Psychogenic movement disorders are usually identified on the basis of (1) unusual motor phenomenology and other clues as listed in Tables 25.2 and 25.3, (2) a discrepancy between the patient’s disability and objective signs of motor deficit, and (3) the presence of psychiatric abnormalities. First, the neurologist bases the suspected diagnosis on identifying the different types of abnormal movements that are present in a given patient. The type of movement disorder is assigned the basis of the phenomenology, which can consist of more than one type (item 5, Table 25.2). The neurologist must exclude possible organic causes for the abnormal movements so that both the neurologist and the patient feel comfortable that the diagnosis of a psychogenic movement disorder has been made with confidence. Then the consulting psychiatrist attempts to establish a psychiatric diagnosis. Finally, a suggested strategy for treatment is presented to the patient. In fact, explaining to the patient that the condition has the potential for a more favorable outcome with proper treatment than would an organic movement disorder may help the patient more readily accept the diagnosis of a psychogenic etiology.
Medically unexplained neurologic symptoms are common. About one-third of neurology outpatients receive that diagnosis (Stone et al., 2009). It would appear that neurologists are quite accurate when diagnosing a psychogenic disorder. Of 1144 patients diagnosed as medically unexplained, by 18 months, only 0.4% had acquired an organic disease diagnosis that was unexpected at initial assessment and plausibly the cause of the patients’ original symptoms (Stone et al., 2009).
The types of psychogenic movements seen in a review of the publications from eight movement disorders centers are presented in Table 25.4. Tremor was found to be the most common psychogenic phenomenology, followed by dystonia. Tics were the least common.
Table 25.4 Predominant movement features in psychogenic movement disorders
| Predominant movement feature | No. | Percent |
|---|---|---|
| Tremor | 467 | 37.5 |
| Dystonia | 365 | 29.3 |
| Myoclonus | 146 | 11.7 |
| Gait disorder | 114 | 9.2 |
| Parkinsonism | 60 | 4.8 |
| Tics | 29 | 2.3 |
| Other | 64 | 5.1 |
| Total | 1245 | 100 |
A tabulation of psychogenic movement disorders seen at eight centers; most centers report their patients by a single primary motor feature, but some report multiple features if more than one is present.
Data from Lang AE. General overview of psychogenic movement disorders: epidemiology, diagnosis, and prognosis. In Hallett M, Fahn S, Jankovic J, et al., eds. Psychogenic Movement Disorders – Neurology and Neuropsychiatry. Philadelphia, Lippincott Williams & Wilkins, 2006; pp. 35–41.
Williams and colleagues (1995) reviewed the records of 131 patients with psychogenic movement disorders and listed their motor phenomenologies (Table 25.5). In their experience, dystonia, tremor, gait disturbances, paroxysmal dyskinesias, and myoclonus were the major motor types that were encountered. The difference from other centers that found tremor to be more common than dystonia may be because the Columbia group labeled movements on a hierarchical scale, whereby if any dystonia is present, regardless if other movements like tremor are also present, the condition was coded as a dystonic one. Williams and colleagues found that 79% of patients had multiple types of abnormal movements and that only 21% had a single definable type (Table 25.6). Moreover, again in contrast with the vast majority of organic movement disorders, in 55% of the patients the movements were either intermittent or paroxysmal, while only 45% of the patients had only continuous movements. They also reported that the onset was abrupt in 60% of patients, usually with a specific inciting event. In 43% of patients, the movements spread beyond the initial site of involvement.
Table 25.5 Principal motor phenomenology in 131 patients with psychogenic movement disorders
| Movements | No. | Percent of organic cases |
|---|---|---|
| Dystonia | 82 | 2.5 |
| Tremor | 21 | |
| Gait disorder | 14 | |
| Myoclonus | 11 | |
| Blepharospasm/facial movements | 4 | |
| Parkinsonism | 3 | <0.1 |
| Tics | 2 | |
| Stiff person | 1 | |
| Paroxysmal and undifferentiated movements | 14 |
Total for types of movements = 152, because more than one type was equally prominent.
Data from Williams DT, Ford B, Fahn S. Phenomenology and psychopathology related to psychogenic movement disorders. Adv Neurol 1995;65:231–257.
Table 25.6 Phenomenology of psychogenic movements
| Single type | 21% |
| Multiple types | 79% |
| Continuous movements | 45% |
| Intermittent/paroxysmal | 55% |
| 15 patients with hand tremor: dominant hand | 93% |
| Abrupt onset (usually inciting event) | 60% |
| Spread from initial site | 43% |
Data from Williams DT, Ford B, Fahn S. Phenomenology and psychopathology related to psychogenic movement disorders. Adv Neurol 1995;65:231–257.
Factor and colleagues (1995) reviewed their 28 cases of psychogenic movement disorders. These represented 3.3% of all 842 consecutive movement disorder patients seen over a 6-year period. Tremor was most common (50%), followed by dystonia, myoclonus, and parkinsonism. Clinical clues included distractibility (86%) and abrupt onset (54%). Distractibility was more important in tremor and least important in dystonia. Other diagnostic clues included entrainment of tremor to the frequency of repetitive movements of another limb, fatigue of tremor, stimulus sensitivity, and a previous history of psychogenic illness.
The demographic pattern of the 131 patients reported by Williams and colleagues (1995) is presented in Table 25.7. Of the 131 patients, 87% were females; the mean age at onset was 37 years, with a range of 4–73 years. An organic component of a movement disorder was present in 13%. The mean duration before a correct diagnosis was made was 5 years.
Table 25.7 Demographics of patients with psychogenic movement disorders
| Age at onset |
Data from Williams DT, Ford B, Fahn S. Phenomenology and psychopathology related to psychogenic movement disorders. Adv Neurol 1995;65:231–257.
An organic diagnosis was made originally in 75% of the patients with a psychogenic movement disorder (Table 25.8), including three patients who carried a diagnosis of multiple sclerosis despite the lack of any positive laboratory data detected by the treating neurologist. A number of neurologic findings presented as clues to psychogenicity. The most common was the presence of give-way weakness (37%). Next most common was a startle reaction that was nonphysiologic (29%). Pain and false sensory findings on examination were also encountered (Table 25.8). Surprisingly, psychogenic seizures were concurrently present in 12% of the patients. The psychogenic movement disorder was disabling in 65% of the patients. A preceding history and inciting event of head trauma and peripheral trauma occurred in 25% and 12.5% of patients, respectively.
Table 25.8 Clinical features in patients with psychogenic movement disorders
| Previously erroneously diagnosed as organic (3 with multiple sclerosis despite negative laboratory tests) | 75% |
| False weakness | 37% |
| False sensory exam | 8.7% |
| Pain & tenderness | 17.4% |
| Startle | 29% |
| Psychogenic seizures | 11.6% |
| Disabled | 65% |
| Head trauma | 25% |
| Peripheral trauma | 12.5% |
Data from Williams DT, Ford B, Fahn S. Phenomenology and psychopathology related to psychogenic movement disorders. Adv Neurol 1995;65:231–257.
Williams and colleagues (1995) found that the most common psychiatric diagnosis was a somatoform disorder, particularly a conversion disorder (Table 25.9). Briquet syndrome (somatization disorder) was diagnosed in 12.5%, and there were even fewer patients with a factitious disorder (8%) or malingering (4%). An accompanying depression or anxiety was found in 71% and 17% of patients, respectively.
Table 25.9 Psychiatric aspects of psychogenic movement disorders
| Conversion disorder | 75% |
| Somatization disorder | 12.5% |
| Factitious disorder | 8.3% |
| Malingering | 4.2% |
| Accompanying | |
| depression | 71% |
| anxiety | 17% |
| Hypnotizable | |
| highly | 36% |
| mild-moderately | 41% |
Data from Williams DT, Ford B, Fahn S. Phenomenology and psychopathology related to psychogenic movement disorders. Adv Neurol 1995;65:231–257.
Psychogenic dystonia
It is, in some ways, ironic that torsion dystonia can sometimes be due to psychogenic causation. From its earliest beginnings, idiopathic torsion dystonia appeared to have been mistaken as a manifestation of a psychiatric disturbance (Schwalbe, 1908). Soon after Schwalbe’s description in 1908 (see English translation by Truong and Fahn, 1988), however, Oppenheim (1911b) and Flatau and Sterling (1911) set matters right by emphasizing the organic nature of this disorder. Although some early publications on dystonia mentioned the “functional” nature of the symptoms (Destarac, 1901) or used the label, neurosis (Ziehen, 1911), these terms were employed in those days in a manner different from today. Functional referred to a physiologic activation of the abnormal movements with voluntary motor activity, which would otherwise disappear when the patient was quiet at rest. Neurosis was a term that was used to indicate a neurologic, rather than a psychiatric, disorder but one without a structural lesion. Today, it is common for the term functional to be equivalent to psychogenic and for neurosis not to be used at all in neurology but to refer to a certain type of psychiatric disorder.
Thus, for many decades, the organic nature of torsion dystonia was emphasized. Yet, possibly beginning in the 1950s, many patients with various forms of focal, segmental, and generalized dystonia began to be misdiagnosed as having a conversion disorder (Table 25.10). Among 44 patients with idiopathic dystonia reviewed by Eldridge and colleagues (1969), 23 patients (52%) had previously been referred for psychiatric treatment (without benefit). Marsden and Harrison (1974) had a similar experience; 43% of their 42 patients were previously diagnosed as suffering from hysteria. Cooper and his colleagues (1976) reviewed their series of 226 patients and found that 56 patients (25%) had a diagnosis of psychogenic etiology at some time during their illness. Lesser and Fahn (1978) reviewed the records of 84 patients with idiopathic dystonia seen at Presbyterian Hospital in New York from 1969 to 1974 and found that 37 patients (44%) had previously been given a diagnosis that their movement abnormalities were due to an emotional disorder. These 37 patients consisted of 11 with generalized dystonia, 14 with segmental dystonia, and 19 with focal dystonia (14 with torticollis, 2 with oromandibular dystonia, and 3 with blepharospasm).
Table 25.10 Reports on the misdiagnosis of organic dystonia as being psychogenic
| Eldridge et al. (1969) | 23/44 (52%) |
| Marsden and Harrison (1974) | 18/42 (43%) |
| Cooper et al. (1976) | 56/226 (25%) |
| Lesser and Fahn (1978) | 37/84 (44%) |
Although some authors (Meares, 1971; Tibbets, 1971) suggested that an underlying psychiatric illness might exist in patients with torticollis, others (Zeman and Dyken, 1968; Cockburn, 1971; Riklan et al., 1976) found no differences between dystonic patients and controls in regard to previous psychiatric history and current life adjustment or on psychiatric testing. Similarly, some authors (Crisp and Moldofsky, 1965; Bindman and Tibbets, 1977) considered hand dystonia (writer’s cramp, occupational cramp) to be psychogenic. But Sheehy and Marsden (1982) studied 34 patients with writer’s or other occupational cramps affecting the hand or arm. All patients underwent assessment by a psychiatric interview technique; these patients compared favorably with a control group, and the investigators concluded that their disorder was not psychiatric in origin. Another recent study involved psychiatric assessment in 20 subjects with focal hand dystonia and also concluded that none had any serious psychopathology (Grafman et al., 1991). Furthermore, patients with writer’s cramp do not have increased anxiety (Harrington et al., 1988).
At the time of the first international symposium on dystonia, held in 1975, Fahn and Eldridge (1976) noted that no case of proven psychological dystonia had been reported. With the realization that patients with dystonia were being misdiagnosed as having a psychiatric disorder, knowledgeable neurologists became sensitive to this problem and, since then, seemed to avoid a diagnosis of hysterical dystonia. However, at the annual meeting of the American Academy of Neurology in 1983, Fahn and colleagues (1983) described ten patients as having documented psychogenic dystonia, five of them identified after the abstract to the meeting was submitted. Batshaw and colleagues (1985) had followed a patient who had been misdiagnosed as having an organic dystonia and who had had a stereotactic thalamotomy based on that diagnosis; these authors eventually recognized that their patient had psychogenic dystonia and reported her as a case of Munchausen syndrome. Fahn and Williams (1988) have described 22 cases of documented or clinically established psychogenic dystonia, including a case of a young girl who underwent a stereotactic thalamotomy. Lang (1995) reported on 18 patients with documented or clinically established psychogenic dystonia, 14 of whom had a known precipitant. Involvement of the legs occurred in 12 patients, despite onset in adulthood. Ten of Lang’s patients had paroxysmal worsening of dystonia or other abnormal movements. Pain was a prominent feature in 14 of 16 patients with this complaint.
Psychogenic dystonia is difficult to diagnose, since there are no laboratory tests to establish the diagnosis of organic idiopathic dystonia. A number of cortical and spinal reflex abnormalities have been reported in organic dystonia, all showing lack of inhibition or spread of cortical field (see Chapter 12). These abnormalities could be a useful way to differentiate psychogenic dystonia from organic dystonia. But when these tests were applied to both groups to see their differences, the results were similar in the two groups, that is, both groups showed a reduced inhibition (Espay et al., 2006). This supports the growing findings detected by PET scans in psychogenic neurologic disorders that the central nervous system accommodates its physiology to follow the motor pattern.
Without laboratory analysis, diagnosis depends on clinical skill to differentiate organic and psychogenic dystonia. The clues listed in Tables 25.2 and 25.3 should help to alert the clinician to the possibility of a psychogenic etiology. Clues that often point to an organic diagnosis, such as a sensory trick (geste antagoniste) that mitigates dystonia, can be very helpful, but also occasionally can be misleading (Munhoz and Lang, 2004).
In a survey of 22 patients reported by Fahn (1994) on documented and clinically established cases of psychogenic dystonia, he found that 6 patients had paroxysmal dystonia, and 16 had continual dystonia. Females outnumbered males by a ratio of 20 : 2. The youngest age at onset was 8 years, and the oldest was 58 years. Those with paroxysmal dystonia were, as a general rule, older than patients with continual dystonia.
Psychogenic nondystonic movement disorders
Psychogenic tremor
As mentioned above, rhythmic movements are the most common abnormal movement in patients with psychogenic movements, often appearing as shaking movements. But what resembles organic tremor is also a common presentation. The tremor tends to be present equally with the affected limb at rest, with posture holding and with action (Video 25.10). This helps differentiate it from organic tremors, which typically dominate in just one of these characteristic features. Also, psychogenic tremor tends to vary in pattern (for example, being vertical in the hands when the arm is at rest, and being horizontal in the hands when the arm is held against gravity in front of the body) (Jankovic et al., 2006b). Distracting the patient with a disappearance of the tremor is a helpful sign that the tremor is psychogenic (Campbell, 1979), but it is not specific enough. Many patients with organic tremor can temporally suppress the tremor, even parkinsonian tremor; furthermore, distractibility is often difficult to observe. Many patients are sophisticated, and it is difficult to eliminate their tremor with distraction. Entrainment of the tremor to a new frequency may sometimes be seen by having the patient touch thumb to the different fingers in a dictated pattern. Of 12 patients with psychogenic tremor compared to 33 with organic essential tremor studied by Kenney and colleagues (2007), psychogenic tremor was significantly more likely to start suddenly and was more likely associated with spontaneous remissions compared to essential tremor; family history of tremor was significantly more common in the essential tremor group, distraction with alternate finger tapping significantly decreased psychogenic tremor, but entrainment did not differentiate the two groups. 
Koller and colleagues (1989) diagnosed 24 patients with psychogenic tremors. They described the tremors as complex; usually they were present at rest, with posture, and with action. The onset was abrupt, and in all but one the tremors lessened or were abolished with distraction. Fahn (1994) described that psychogenic tremors are sometimes paroxysmal and not always continuous. Deuschl and colleagues (1998) reviewed 25 cases of psychogenic tremor. Sudden onset and rare remissions were common. The “coactivation sign” and absent finger tremor were the most consistent criteria to separate them from organic tremors. Whereas most organic tremors show decreasing amplitudes when the extremity is loaded with additional weights, most psychogenic tremors show an increase of tremor amplitude (i.e., coactivation sign). Overall, psychogenic tremor in their series had a poor outcome. Kim and colleagues (1999) reviewed their series of 70 cases of psychogenic tremor. They emphasized the abrupt onset (73%), often with the maximal disability at onset (46%), and then taking static (46%) or fluctuating (17%) courses. Tremor usually started in one limb and spread rapidly to a generalized or mixed distribution. Other features were spontaneous resolution and recurrence, as well as easy distractibility together with entrainment and response to suggestion. McKeon and colleagues (2009) followed up their 62 patients with psychogenic tremor; 33 responded. The outcome was good (mild or no tremor) in 36%, moderate in 24% and severe in 40%. Five patients with the good outcome had spontaneous improvement without psychotherapy.
In addition to tremor in the limbs, psychogenic palatal tremor has been reported (Pirio Richardson et al., 2006). Psychogenic stridor was diagnosed in a boy who developed inspiratory stridor when trying to fall asleep (Vetrugno et al., 2009), but this seems more appropriately to be called anxiety-induced stridor.
Another electrophysiologic approach to aid in distinguishing between psychogenic and organic tremors is with accelerometry. Tremor is measured in one hand while the other hand either rested or tapped to an auditory stimulus at 3 and 4 or 5 Hz. Psychogenic tremors showed larger tremor frequency changes and higher intraindividual variability during tapping (Zeuner et al., 2003). Motor control physiology can be useful to distinguish psychogenic from organic tremor (Deuschl et al., 2006).
About half of the psychogenic tremors are coherent between the two arms, suggesting to the authors that coherent tremors might be voluntary, while noncoherent tremors are involuntary (Raethjen et al., 2004). Voluntary tapping of the contralateral limb usually results in either dissipating the tremor or shifting the tremor frequency to that of the metronome (O’Suilleabhain and Matsumoto, 1998).
A patient who underwent deep brain stimulation for the treatment of essential tremor developed psychogenic tremor following the surgery (McKeon et al., 2008).
Psychogenic gait
An abnormal gait is a common feature in patients with a psychogenic movement disorder. Of 279 patients, 118 (42%) had an abnormal gait (Baik and Lang, 2007). 102 (86%) of these 118 patients had other psychogenic movements, and gait was also abnormal, with slowing of gait (18.6%), dystonic gait (17.8%), bizarre gait (11.9%), astasia–abasia (11.9%), and buckling of the knee (7.6%) as the most common types. Among the pure psychogenic gait disorders, buckling of the knee was the most common feature (31.3%), followed by astasia–abasia (18.8%) (Table 25.11).
| Clinical feature | Mixed type | Pure type |
|---|---|---|
| Number of patients | 102 | 16 |
| Slowing | 21 | 1 |
| Dystonic | 20 | 1 |
| Bizarre | 12 | 2 |
| Astasia–abasia | 11 | 3 |
| Knee-buckling | 4 | 5 |
| Tight-rope walking | 7 | 1 |
| Trembling | 4 | 1 |
| Stiff-legged | 5 | 0 |
| Dragging | 4 | 0 |
| Scissoring | 4 | 1 |
| Truncal myoclonus | 4 | 0 |
| Fatigue | 3 | 0 |
| Waddling | 2 | 1 |
| Ataxic | 1 | 0 |
Data from Baik JS, Lang AE. Gait abnormalities in psychogenic movement disorders. Mov Disord 2007;22(3):395–399.
Morris and colleagues (2006) described key features of the psychogenic gait. These include exaggerated effort, fatigue with groans and sighs, extreme slowness, appearance of pain with grimaces, knee-buckling, unusual postures, and astasia–abasia. Keane (1989) described 60 cases with psychogenic gait abnormality out of 228 patients with psychogenic neurologic problems. Among these abnormal gaits were 24 patients with “ataxia” (the most common gait abnormality), 9 patients with trembling, 2 patients with “dystonia,” 2 patients with truncal “myoclonus,” and 1 patient with camptocormia (markedly stooped posture). Among the myriad of associated psychogenic signs were 8 patients with tremor. A knee giving way, with recovery, was seen in 5 patients, and is a feature of a case that presented as an unknown, unusual movement disorder (Vecht et al., 1991). In a video review of psychogenic gaits, Hayes and colleagues (1999) emphasized certain features of the gait: exaggerated effort, extreme slowness, variability throughout the day, unusual or uneconomic postures, collapses, convulsive tremors, and distractibility. On the other hand, it is possible to misdiagnose as psychogenic an abnormal gait that is organic. Such happened to a patient with a gait disorder and episodic weakness that were thought to be psychogenic who was subsequently diagnosed with status cataplecticus due to narcolepsy (Simon et al., 2004).
Fear of falling
According to Keane (1989), Spiller (1933) referred to the syndrome of fear of falling as staso-basophobia. Fear of falling is a syndrome in which the patient can walk perfectly well if he or she is holding onto someone, but is unable to walk without leaning against furniture or walls if alone. Sometimes, this could be purely due to a psychiatric problem, such as agoraphobia. Most of the patients we have seen with this problem developed the condition after they had fallen, usually from organic causes (such as loss of postural reflexes or ataxia) and were left with a marked fear of falling when walking without holding on. One of our patients with essential action myoclonus developed this disorder after suffering several falls and continued to have fear of falling even after successful treatment of the myoclonus with clonazepam. The freezing phenomenon (or motor blocks) that is seen in parkinsonism and the gait in action myoclonus patients are the other major conditions in which the gait also normalizes when the patient holds on to someone. The fear-of-falling syndrome is usually separated from the list of psychogenic movement disorders (see below), and would be characterized as a psychiatric movement disorder. But in many of these patients, the fear of falling is beyond what is rational, so there is a psychogenic component. Women are more affected than men, and often the mistaken diagnosis is Parkinson disease (Kurlan, 2005).
Psychogenic myoclonus
Psychogenic myoclonus should be relatively easy to distinguish from organic myoclonus if access to a motor control physiology laboratory is available (Brown, 2006). PolyEMG is very helpful in distinguishing psychogenic myoclonus from organic myoclonus. The short duration of a myoclonic jerk (usually less than 100 ms) is almost impossible to duplicate voluntarily. The EMG pattern of voluntary jerks exhibits a triphasic pattern of activity between antagonistic muscles, whereas cortical myoclonus consists of short-duration 25–50 ms bursts of cocontracting antagonists muscles (Thompson, 2006). Furthermore, the latency of reflex myoclonus is physiologically short (40–100 ms) whereas abnormal reactive voluntary jerks are much longer (Thompson, 2006).
Monday and Jankovic (1993) reported 18 patients with psychogenic myoclonus (although no EMG observations were reported to indicate that myoclonus was the actual type of abnormal movement), stating that this is the most common form of psychogenic movement disorder encountered in their clinic. The myoclonus was segmental in 10 patients, generalized in 7 patients and focal in 1 patient. Psychogenic myoclonus accounted for 8.5% of the 212 patients with myoclonus in their clinic. Inconsistency with continuously changing pattern anatomically and temporally was common. The movements often increased with stress, anxiety, and exposure to noise or light. A Bereitschaftspotential preceding muscle jerks was found in five of six patients with a diagnosis of psychogenic myoclonus (Terada et al., 1995). The authors suggest that this is a positive sign for the diagnosis of psychogenic myoclonus, but because of the one patient who did not have a Bereitschaftspotential, its absence cannot be used to exclude the diagnosis.
Rhythmical palatal myoclonus has also been reported to be of a psychogenic etiology in rare cases (Williams, 2004; Pirio Richardson et al., 2006). A case of propriospinal myoclonus was presumed be of psychogenic etiology when it disappeared after some minor procedures (Williams et al., 2008).
Psychogenic tics
Psychogenic movements can sometimes resemble tics, but these are one of the least common manifestations of a psychogenic movement disorder (Lang, 2006). It is more complicated when organic tics are also present. Dooley and colleagues (1994) described two children with Tourette syndrome who also had pseudo-tics, in whom the psychogenic movements resolved when the stressful issues in their lives were addressed.
Psychogenic parkinsonism
Psychogenic parkinsonism is relatively uncommon (see Tables 25.4 and 25.5). Lang and colleagues (1995) reported 14 patients with this disorder. Eleven patients had tremor at rest, but the tremor did not disappear with movement of the limb, and the frequency and rhythmicity varied. Rigidity was present in six patients but without cogwheeling. All 14 patients had slowness of movement (bradykinesia) without the typical decrementing feature of organic bradykinesia (Video 25.11). One patient had evidence of some organic parkinsonism as well but required a fluorodopa PET scan to be certain. Other studies also reported the combination of organic and psychogenic parkinsonism and found the dopaminergic SPECT imaging can help in distinguishing this diagnosis from pure psychogenic parkinsonism (Benaderette et al., 2006; Gaig et al., 2006). 
Approaches to the patient suspected of having a psychogenic movement disorder
Results of treatment
Psychotherapy is the major treatment approach that is best suited for permanent benefit. Somatoform disorders have the best results from treatment. Factitious disorders and malingering yield poor results, and the patient improves only when he or she is ready to relinquish the symptoms. Williams and colleagues (1995) utilized psychotherapy in all patients, along with the following supplemental approaches: family sessions, 58%; hypnosis, 42%; physical therapy, 42%; and placebo therapy, 13% (Table 25.12). Psychotropic medication (antidepressants) was utilized in 71%. Two patients with treatment-resistant major depression received ECT; one responded completely, and the other responded only partially. One-quarter of the patients required more extensive psychiatric hospitalization because of suicidal ideation or because there was a poor response in reversing the psychodynamic pathology while on the neurology service.
| Accepted diagnosis and treatment | 70% |
| Refused diagnosis and treatment | 30% |
| Psychiatrically treated patients | |
| Family sessions | 58% |
| Hypnosis | 88% |
| Physiotherapy | 42% |
| Placebo | 13% |
| Antidepressants | 71% |
| ECT | 8% |
Data from Williams DT, Ford B, Fahn S. Phenomenology and psychopathology related to psychogenic movement disorders. Adv Neurol 1995;65:231–257.
Treatment by Williams and colleagues (1995) resulted in a permanent, meaningful benefit in 52% of patients, with complete relief, considerable relief, and moderate relief in 25%, 21%, and 8% of patients, respectively (Table 25.13). Some relapse occurred in 21% of patients, and no improvement was seen in 12%. Of those who had been previously employed, 25% were able to resume full-time work, and 10% were able to work part-time, with 15% functioning at home (see Table 25.13).
Table 25.13 Results of treatment of psychogenic movement disorders
| Permanent, complete relief | 25% |
| Permanent, considerable relief | 21% |
| Permanent, moderate relief | 8% |
| Relapse | 4% |
| Partial relapse | 17% |
| No improvement | 12% |
| Previously employed | |
| Now working full-time | 25% |
| Now working part-time | 10% |
| Functioning at home | 15% |
| Now disabled | 30% |
Data from Williams DT, Ford B, Fahn S. Phenomenology and psychopathology related to psychogenic movement disorders. Adv Neurol 1995;65:231–257.
In the series of 28 cases of psychogenic movement disorders reported by Factor and colleagues (1995), 35% resolved, and this subgroup had a shorter duration of disease than those who did not resolve. Of 56 patients with any type of psychogenic neurologic disorder other than pseudoseizures, Couprie and colleagues (1995) found that the long-term outcome was good in 96% of those who improved during a hospital stay and in only 30% of others, and that rapid improvement was related to recent onset of symptoms. In a longitudinal study of 228 patients evaluated in the Baylor College of Medicine Movement Disorders Clinic, after a mean duration of follow up of 3.4 ± 2.8 years, improvement of symptoms was noted in 56.6% patients, 22.1% were worse, and 21.3% remained the same at the time of follow-up. Positive social life perceptions, strong suggestion by the physician of effective treatment, elimination of stressors, and treatment with antidepressant medications contributed to a favorable outcome. Using a “blinded” review of videos, psychiatric rating scales, and psychogenic movement disorder scale, Hinson and colleagues (2006) demonstrated the efficacy of psychotherapy and medications in the treatment of patients with psychogenic movement disorders.
We can compare treatment of psychogenic movement disorders with that of psychogenic nonepileptiform seizures. In a double-blind study, cognitive-behavioral therapy was more effective than standard medical care in reducing seizure frequency in these patients (Goldstein et al., 2010). This contrasts with limited or no special treatment. About one-third became seizure free, one-sixth worsened, and the others were unchanged (McKenzie et al., 2010).
Movement disorders caused by psychiatric conditions but not regarded as psychogenic
A number of movement disorders are due to diseases that are classified as mental or psychiatric disturbances, in which the abnormal hypokinesia or hyperkinesia is not listed as a psychogenic movement disorder. Table 25.14 lists these, as well as the common underlying causes.
Table 25.14 Movement disorders that are symptoms of psychiatric conditions and not classified as psychogenic movement disorders
| Psychiatric condition | Psychiatric movement disorder |
|---|---|
| Schizophrenia, depression | Catatonia |
| Depression | Psychomotor slowness |
| Obsessive-compulsive disorder | Obsessional slowness, stereotypies |
| Agoraphobia, anxiety | Fear of falling |
| Schizophrenia, autism | Stereotypies |
Table 25.14 shows that, basically, none of the aforementioned psychiatric conditions is either a somatoform disorder, a factitious disorder, or a malingering state. Thus, we can distinguish the psychogenic movement disorders from the conditions listed in Table 25.14 on the basis of the underlying psychiatric state. It should be noted that even if a somatoform disorder, a factitious disorder, or a malingering state is only suspected and not officially diagnosed, the diagnosis of a psychogenic movement disorder can still be made. Also, even if a psychiatric consultant cannot detect one of these disorders, a neurologist may still make the diagnosis on the grounds listed in Tables 25.2 and 25.3.
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