Viewpoint

Electrophysiological Aids to the Diagnosis of PsychogenicJerks, Spasms, and Tremor

Peter Brown, MD, FRCP1* and Philip D. Thompson, MD, FRACP2

1MRC HMBU, The Institute of Neurology, Queen Square, London, United Kingdom2The University Department of Medicine and Department of Neurology, Royal Adelaide Hospital, Adelaide, Australia

Retrospective surveys of specialist movement disorderclinics suggest that 2.1% to 3.3% of patients have psy-chogenic movement disorders.1,2 Some movement disor-ders are more likely to be psychogenic than others.Around 60% of nonfamilial, idiopathic paroxysmal dys-kinesias are psychogenic,3 whereas less than 0.5% ofcases of parkinsonism and chorea attending specialistmovement disorder clinics are psychogenic.1,2 Withinthe setting of a specialist clinic, tremor, jerks, or abnor-mal limb postures comprise the majority of psychogenicmovement disorders. In our experience, as in that ofothers, up to 10% of tremor and myoclonus cases have apsychogenic aetiology.1,4,5

Fifty percent of patients with a psychogenic move-ment disorder (PMD) improve to a degree. Only one-third resolve. These patients tend to have a shorter du-ration of movement disorder, suggesting that early diag-nosis and treatment may be important.2 At the same time,erroneous diagnoses of PMD may lead to important de-lays in the treatment of nonpsychogenic diseases, as wasthe case for the dystonias in the past. It also is importantto note that 25–30% of patients with PMD have a coex-isting nonpsychogenic movement disorder or other neu-rological disease.2,6

Clinical Features of PsychogenicMovement Disorders

Clinical features suggestive, but not diagnostic, of apsychogenic origin are the sudden onset of an inconsis-

tent and variable movement disorder. Additional cluesare the lessening of movements when distracted and,conversely, a dramatic increase in severity and complex-ity of movements during by direct observation, settlingagain when no longer under direct observation. The ab-sence of signs of organic neurological disease and theunusual nature of the movements are also suggestive, butnot necessarily diagnostic of a psychogenic aetiology.More convincing is the disappearance of the movementdisorder when supposedly unobserved or following sug-gestion and placebo. The typical indicators of a conver-sion disorder, such as psychological precipitants, mul-tiple somatisations, and secondary gain may or may notbe present. Psychological factors are only discovered inone-third of patients with somatisation in general neuro-logical practice,7 and are, of course, not limited to thosewith psychogenic disease. Moreover, the distinction be-tween primary psychological factors and those secondaryor consequent to illness can be difficult. A definite di-agnosis of PMD may therefore be hard to achieve onclinical grounds. Often no more than a suspicion of apsychogenic movement disorder is possible, leading to aprotracted “wait-and-see” management policy. This isparticularly so, given the increasing breadth of pheno-types of confirmed organic movement disorders. Accord-ingly, it is uncommon to find a PMD that is totally in-congruent with a recognised movement disorder, a pointacknowledged as one of the principal diagnostic criteriain existing classifications of PMD (Table 1A). It shouldalso be emphasised that movement disorders should notbe diagnosed as hysterical “for no better reason that theyare not yet officially described,” a point elegantly madeby Asher.8 Recent advances in the electrophysiologicalassessment of movement disorders, coupled with a

*Correspondence to: Dr. P. Brown, MRC Human Movement andBalance Unit, Institute of Neurology, Queen Square, London, WCIN3BG, United Kingdom. E-mail: p.brown@ion.ac.uk

Received 10 September 2000; Revised 30 November 2000; Ac-cepted 11 December 2000

Published online 11 July 2001; DOI 10.1002/mds.1145

Movement DisordersVol. 16, No. 4, 2001, pp. 595–599© 2001 Movement Disorder SocietyPublished by Wiley-Liss, Inc.

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greater understanding of the pathophysiology of move-ment disorders, have identified a number of characteris-tic physiological changes in many movement disorders.As discussed below, the use of these tests also providesone method of identifying patterns of movement thatcould be under voluntary control, and thereby contributestowards the positive diagnosis of PMD. Such tests permitfurther refinement of the classification of PMD first sug-gested, and subsequently adapted, by Fahn and col-leagues.1,9,10

JerksA particularly difficult clinical problem can be the

separation of psychogenic jerks from tics and myoclo-nus. Taking simple surface electromyographic (EMG)recordings from the muscles producing the movements isa useful initial step. Jerks due to bursts of EMG activitywith a mean duration less than 70 ms are likely to beorganic, particularly when there is cocontraction of ago-nist and antagonist muscle pairs. Conversely, jerks withlonger EMG bursts, especially if there is a well-organised triphasic pattern of activation of agonist andantagonist muscles, are more likely to be psychogenic.However, these features alone are insufficient to make adiagnosis of PMD and more specific electrophysiologi-cal investigations are required. Such investigations de-pend on whether movements are spontaneous or evokedby a stimulus such as sound or tap.

Spontaneous JerksEvidence for the aetiology of spontaneous jerks is

sought by examining electroencephalographic activity

(EEG) preceding the jerks, using the technique of back-averaging epochs of EEG preceding the EMG accompa-nying spontaneous jerks. Self-initiated voluntary move-ments are normally preceded by a premovement poten-tial, the Bereitschafspotential. This is a slow positivepotential beginning around one second prior to move-ment and maximal over the vertex.11–14 Similar poten-tials are also found preceding spontaneous psychogenicjerks.12,15 In contrast, a slow premovement potentialdoes not precede organic spontaneous myoclonus, al-though a much briefer cortical spike discharge or sharpwave may precede cortical myoclonus by an interval of20–40 ms, depending on whether the muscle under in-vestigation is in the upper or lower limb.16

The majority of patients with tics also do not exhibit apremovement potential prior to involuntary move-ments,12,17although a few have an abbreviated premove-ment potential, similar to the later and steeper componentof the normal premovement potential.14 An abbreviatedpremovement potential has also been described in themyoclonus accompanying dystonia.18 This is in contrastto the chorea of choreoacanthocytosis, where premove-ment potentials may be recorded.19

However, the technique of back-averaging has severalmethodological limitations. The poor signal-to-noise ra-tio requires collecting and averaging at least 40 trials.Accordingly, when movements are infrequent, the valueof the technique is limited particularly if there are timeconstraints. Conversely, averages are unreliable whenmovements occur more often then every 2 seconds. Un-der these circumstances, frequency analysis may be a

TABLE 1B. Combined clinical and electrophysiological classification of PMD

Grade Combined clinical and electrophysiological classification

Definite PMD MD that disappears when supposedly unobserved or after psychotherapy, suggestion or placebo.Spontaneous jerks preceded by a premovement potential.**Pathological tremor that is entrainable, confirmed electrophysiologically

Probable PMD MD in association with other related features.*Tremor that increases in amplitude with loading or is only seen in the presence of coactivation.

Possible PMD MD that is inconsistent over time or with a recognised MD, but other related features lacking.*

*Psychogenic signs, multiple somatisations, psychiatric disturbance, and/or excessive slowness of movement.**Those with an abbreviated premovement potential are excluded, as this may sometimes be seen in tics.14

MD, movement disorder; PMD, psychogenic movement disorder.†Note that definite, probable, or possible PMD may occur in combination with organic neurological disease, including

other movement disorders.

TABLE 1A. Clinical classification of PMD

Grade Fahn and Williams clinical classification9,10

Clinically definite PMD† MD that disappears when supposedly unobserved or after psychotherapy suggestion or placebo.MD that is inconsistent over time or incongruent with a recognised MD, in association with other related features.*

Probable PMD MD that is inconsistent over time or with a recognised MD, but other related features lacking.*MD that is consistent over time and congruent with a recognised MD, but seen with other related features.*

Possible PMD MD plus emotional disturbance

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more appropriate technique.20 Neither technique may beuseful if many head and facial movements are made.14

Nevertheless, the presence of a premovement potentialprior to spontaneous abnormal movements is good evi-dence the movements are generated by voluntary effortand are psychogenic. The presence of an abbreviatedpremovement potential is more difficult to interpret. Theabsence of any premovement potential suggests thatspontaneous movements have an organic basis, with onemajor caveat. A premovement potential is absent or ab-breviated when healthy subjects deliberately makemovements in response to an external triggering stimu-lus.13 Thus, care must be taken to avoid cues that mightform the trigger for seemingly spontaneous jerks in psy-chogenic myoclonus and tics.

Reflex Jerks

Reflex myoclonus or jerks that occur in response tovarious stimuli are investigated by recording the latencyof reflex activity after each stimulus. This simple methodis very useful in distinguishing between a true reflexresponse and a reaction to a stimulus occurring in thesetting of pyschogenic illness. The latency of reflex jerksmay also help identify the site of origin of the jerks in thenervous system. Stimulus-evoked jerks or jumps with amean latency in excess of 100 ms suggest voluntary orpsychogenic jerks (Table 2). In addition, the presence ofgiant cortical somatosensory-evoked potentials, short-duration EMG bursts, or characteristic descending pat-terns of muscle recruitment point towards cortical my-oclonus.21 The patterns of stimulus “contingent” EMGactivity provide further clues with long-duration musclebursts, and variable patterns of muscle activation arepresent. None of these characteristics can be considereddiagnostic of a psychogenic aetiology, but most organicreflex myoclonic or startle syndromes are readily sepa-rated on electrophysiological grounds. The stereotypednonhabituating early response in sternocleidomatoid to

sound or tap to the mantle region distinguishes a patho-logical enhancement of the startle response or hyperek-plexia from a voluntary jump.21 It is worth noting thatpatients with PMD may still have a normal startle reflexof short latency, but this rapidly habituates with repeatedstimuli, leaving only psychogenic jerks.

Tremor

Physiological tremor may be enhanced by anxiety, butwe would not consider this a psychogenic tremor. Themost important electrophysiological signs of psycho-genic tremor relate to the difficulty in voluntarily main-taining two or more unrelated rhythms in different bodyparts.22 Thus, the simultaneous occurrence in separatemuscle groups of tremors with different frequencies,(frequency dissociation) is strongly suggestive of organictremor. The absence of frequency dissociation does notnecessarily rule out an organic aetiology.23 It is also verydifficult to maintain a voluntary oscillatory limb move-ment at the same frequency for any length of time. Simi-larly, the ability to entrain tremor is increasinglyrecognised as characteristic of psychogenic tremor.When asked to tap out a beat with the limb contralateralto the tremulous limb under examination, tremor in thelatter either dissipates or shifts to the frequency of tap-ping.1,23,24 Sometimes brief periods of tapping are ob-served to alternate with shuddering displacements of thesymptomatic limb. When gross, frequency dissociationand entrainability can be determined clinically. In lessstriking examples, these characteristics can be confirmedby polymyography and time-frequency and pure fre-quency domain measures,23,24but it should be noted thatphysiological tremor may be entrained to a minor degree.

There are a number of other characteristics helpful inmaking a diagnosis of psychogenic tremor. Patients withpsychogenic tremor may have some underlying coacti-vation of antagonist muscles of the tremuluous joint,which may be detected clinically or electrophysiologi-cally.25 Organic tremor can occur without such coacti-vation. An increase in tremor amplitude with loading issuggestive of psychogenic tremor and is not seen in es-sential or parkinsonian tremor.25 However, some patientswith psychogenic tremor may fail to show this phenom-enon, while some patients may elaborate upon a nonpsy-chogenic tremor, giving mixed results.25 Psychogenictremor tends to have a more variable frequency thanorganic tremor, but overlap between the groups meansthat this is not a useful distinguishing feature in indi-vidual cases.23,26 Tremor bursts of very short durationare likely to be organic, although voluntarily inducedclonus in the lower limb may have a mean burst duration

TABLE 2. Reaction times for voluntary generalised flexionjerks in eight healthy subjects in response to different stimuli.

Sternocleidomastoid Biceps Tibialis anterior

Auditory 115 110 155(81–140) (76–138) (127–180)

Tap knee 122 116 153(90–153) (93–146) (125–192)

Tap radius 113 116 148(89–138) (83–169) (122–181)

Shock to median 137 118 163nerve at wrist (104–176) (97–141) (133–189)

Values are the mean and range of latency to onset of electromyo-graphic (EMG) activity in ms. Each stimulus was presented nine times.Published with permission.21

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of as little as 80 ms (personal observation). Finally, theupper frequency limit of voluntary tremor is 11 Hz,27 andany tremor that is faster than this is very likely to have anorganic aetiology.

Spasms

Psychogenic dystonia is uncommon.1,2 In contrast toidiopathic torsion dystonia, which usually begins withaction dystonia, in which the twisted posture is oftenmobile and accompanied by jerks, psychogenic dystoniais often characterised by a fixed, immobile posture.There may be a reduction in overall capacity for move-ment in the affected limb. As recently reviewed by Be-rardelli et al.,28 a number of electrophysiological abnor-malities have been reported in dystonia, but the specific-ity and sensitivity of these findings limits their use asdiagnostic tests or in excluding a psychogenic disorder inindividual patients. Of these, two tests show promise, butrequire further evaluation. The findings of diminishedreciprocal inhibition in the forearm flexor muscles atintermediate (around 15 ms) and long latencies (around100 ms), when considered together, discriminate patientswith dystonic torticollis from relaxed control subjects.29

Differences may be even more marked when dystoniainvolves the upper limb.30–32However, difficulties arisewhen the abnormal posture persists at rest, as the effectof voluntary contraction mimicking dystonic posturinghas not been systematically analysed. There is also thepossibility that the absence of broad-peak synchronisa-tion of cocontracting antagonist muscles, and of abnor-mal low-frequency common drives to agonist muscles,may serve to distinguish functional from dystonic cocon-tractions.33,34 For example, in a recent study, it wasshown that the finding of an abnormal low-frequencycommon drive manifest as significant coherence betweensternocleidomastoid and splenius capitis EMG in the 4–7Hz band was 90% specific and sensitive for dystonictorticollis.34

Muscle spasm of central origin may also be seen in thestiff people syndromes. These are most simply distin-guished from dystonia by the axial predominance, per-sistence of abnormal postures while at rest, and the pres-ence of stimulus-evoked exacerbations. Reflex spasmscan be of very short latency in the stiff man syndromeand take the form of exaggerated exteroceptive reflexes,which are dramatically enhanced by repetitive stimula-tion. They may be recorded in axial muscles followingstimulation of an upper or lower limb nerve. Otherspasms in the stiff man syndrome include enhanced re-sponses to auditory stimuli with a stereotyped pattern ofmuscle recruitment.35–37 The failure of spontaneous ac-tivity to disappear whenever the corresponding antago-

nist muscles are voluntarily activated helps distinguishboth dystonia and the stiff people syndromes from psy-chogenic spasm.

Conclusion

Psychogenic movement disorders are a significantclinical problem, usually necessitating extensive andsometimes repeated investigation, and are associatedwith a relatively poor prognosis, particularly when diag-nosis is delayed. Recent electrophysiological advanceshave made the positive diagnosis of PMD easier, as re-flected in our refinement of the Fahn classification ofPMD, shown in Table 1B. Yet the electrophysiologicaltechniques discussed here are not widely available. Thisargues in favour of the provision of supraregional centersfor the electrophysiology of complex movement disor-ders, allowing diagnosis and appropriate management ininstances where this might otherwise be impossible, andproviding an opportunity for the development and evalu-ation of further electrophysiological tests.

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