Psychogenic movement disorders
Amitabh Gupta and Anthony E. Lang
Movement Disorders Unit, Toronto Western Hospital,
University of Toronto, Ontario, Canada
Correspondence to Dr Anthony E. Lang, MD, FRCPC,
Director, Movement Disorders Unit, Toronto Western
Hospital, 399 Bathurst Street, McLaughlin 7-418,
Toronto M5T 2S8, Ontario, Canada
Tel: +1 416 603 6422; fax: +1 416 603 5004;
e-mail: lang@uhnres.utoronto.ca
Current Opinion in Neurology 2009, 22:430–436
Purpose of review
This review summarizes the progress made in the area of psychogenic movement
disorders (PMDs) over the past 2 years, and a simplified classification of diagnostic
certainty is proposed that incorporates electrophysiological assessment.
Recent findings
Functional magnetic resonance imaging studies have demonstrated altered blood flow
in conversion disorders that may reflect changes in synaptic activity.
Electrophysiological testing shows limitations in distinguishing between psychogenic
and organic propriospinal myoclonus and dystonia. Recent evidence cautions against
the uncritical acceptance of all cases of posttraumatic myoclonus and ‘jumpy stump’ as
being organic in nature. ‘Essential palatal tremor’ is recognized as a rather
heterogeneous group of tremors that includes psychogenic tremor. Two recent studies
evaluating the long-term prognosis of psychogenic tremor differ in the degree of
unfavorable outcome. Different groups of PMDs might have distinctive gait
characteristics with prognostic, diagnostic, or therapeutic value. Two recent reviews
provide comprehensive information on the understudied area of PMDs in children.
Summary
The diagnosis of PMDs should not be regarded as a diagnosis of exclusion. Careful
clinical assessment is critical, and imaging or electrophysiological studies may provide
important insights and confirmation of the diagnosis though some cases remain
challenging and current assessments fail to provide needed clarification. Treatment is
often delayed, contributing to a largely unfavorable long-term outcome. Well designed
randomized control trials that validate and compare therapeutic options are urgently
required.
Keywords
children, diagnosis, investigations, movement disorders, psychogenic, treatment
Curr Opin Neurol 22:430–436
ß 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
1350-7540
Introduction
Psychogenic movement disorders (PMDs) are movement
disorders that result from a psychological or psychiatric
rather than neurological disturbance. The primary psychiatric diagnosis varies; most cases are considered to be
conversion disorders, in which the problem is caused by
an unconscious mechanism, but infrequently some are
factitious disorders or malingering, in which the abnormal
movements are purposefully feigned. Traditionally,
PMDs represented a diagnosis of exclusion. This perception was fuelled by the observation that PMDs can mimic
various organic diseases, sometimes with confounding
test results [1], and by studies and experiences of high
false positive rates [2–4]. Over the years, stricter clinical
criteria, improved imaging, and investigational advances
have allowed the diagnosis of PMDs to be made more
comfortably [5], and organic movements are far less
often misdiagnosed as psychogenic. Here, we review
1350-7540 ß 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
the literature of the past 2 years and summarize how
PMDs are currently diagnosed, investigated, and treated.
Diagnosis
Although no single clinical finding is pathognomonic for
PMDs, several features are quite helpful. The clinical
aspects of specific types of PMDs (i.e. tremors, myoclonus, dystonia, Parkinsonism, gait disorders) have been
reviewed at length elsewhere [6–8]. Table 1 [8,9] provides a list of typical historical and clinical clues to the
diagnosis.
Over a decade ago, criteria were proposed for various
levels of diagnostic certainty of PMDs [10]. With the
subsequent progress made in establishing clinical characteristics and investigational methods, it appears timely
to propose modifications to the diagnostic classification, including the incorporation of electrophysiological
DOI:10.1097/WCO.0b013e32832dc169
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Psychogenic movement disorders Gupta and Lang 431
Table 1 Clues suggesting psychogenic cause
Historical
Abrupt onset (symptoms often maximal at that time)
Static course
Spontaneous remissions/cures
Paroxysmal symptoms (generally nonkinesigenic)b
Psychiatric comorbiditiesc
Secondary gain (often not apparent)
Risk factors for conversion disorderd
Psychological stressorse
Multiple somatizations/undiagnosed conditions
Employed in allied health professions (infrequent)
General examination
Movement inconsistent
Variability over time (frequency, amplitude, direction/distribution of movement)
Distractibility reduces or resolvesa, attention increases movement
Selective disability
Entrainment (especially with tremor)
Movement incongruous with organic movement disorders
Mixed (often bizarre) movement disorders
Paroxysmal attacks (including pseudoseizures)
Precipitated paroxysms (often suggestible/startle)
Suggestibilityf
Effortful production or deliberate slowness (without fatiguing) of movement
Self-inflicted injury (caution: tic disorders)
Delayed and excessive startle response to a stimulus
Burst of verbal gibberish or stuttering speechg
False (give-away) weakness
Nonanatomical sensory loss or spread of movement
Certain types of abnormal movements common in individuals with PMDsh
Functional disability out of proportion to examination findings
a
Distractibility should be tested both with mental and motor tasks. Although most often organic movement disorders are not suppressed, organic tics or
akathisia can be suppressible, and recently it was shown that diaphragmatic tremor was suppressed by simple motor tasks, perhaps by interference
with central nervous system circuitry [9].
b
Separation from organic paroxysmal dyskinesias can be challenging, particularly if they occur infrequently with prolonged symptom-free periods.
c
Psychiatric diseases can also coincide with organic illness or present as part of the organic movement disorder.
d
Sexual and physical abuse, trauma.
e
Often initiated by injury (often minor) or motor vehicle accident associated with litigation or compensation.
f
Application of pressure with finger or tuning fork may reduce symptom. With paroxysmal symptom, suggestibility and placebo trial may not be helpful,
unless repeated reversals with placebo are documented when symptom otherwise is frequent and attacks are prolonged.
g
Particularly if the entire word is repeated (typically broken up into syllables, each repeated), rather than the initial syllable.
h
Such movements include dystonia that begins as a fixed posture (particularly if abrupt onset, painful, and early contractures are seen); bizarre gait;
twisting facial movements that move mouth to one side or the other (organic dystonia of the facial muscles usually does not pull the mouth sidewise).
Adapted from [8].
techniques (Table 2) [10–12]. The remainder of this
review will discuss recent diagnostic and therapeutic
approaches, with an emphasis on developments in the
areas of investigational methods, posttraumatic movement disorders, psychogenic tremor, psychogenic gait
disorders, and PMDs in children.
Investigations
Nuclear imaging, in contrast to magnetic resonance imaging (MRI), has proven quite helpful in distinguishing
psychogenic Parkinsonism from Parkinson’s disease.
Well established methods include fluorodopa positron
emission tomography (FDOPA-PET), bCIT single
photon emission computed tomography (SPECT)
[13,14], and, recently also, 123I-Isoflupane SPECT
[15]. As these methods detect the degree of viable
dopaminergic neurons of the substantia nigra (PET) or
their respective synaptic termini in the striatum
(SPECT), scan results are normal in psychogenic cases
but show diminished signal in Parkinson’s disease.
Although it has been suggested that nuclear imaging
may be normal in some early cases of Parkinson’s disease,
recent evidence suggests that most of these cases are
likely falsely classified [16]. Therefore, nuclear imaging
may be extremely useful in distinguishing psychogenic
Parkinsonism from Parkinson’s disease.
Functional MRI (fMRI) imaging of conversion disorders
has provided interesting insights into the condition.
Patients with motor conversion disorders (MCDs) have
been shown to activate the motor cortex in a pattern that
differs from controls simulating weakness [17].
Although this suggests that cerebral activity is changed
in MCD, comparison to organic weakness requires elucidation. Similarly, in patients with a sensory conversion
disorder, fMRI has demonstrated that vibratory stimulation of the affected limb fails to activate the contralateral cortical sensory area. This result supports the
notion that clinical deficits in this psychiatric condition
are associated with real changes in blood flow that
indicate reduced cortical responsiveness. The mechanism underlying these changes is not well understood, but
cortical activation was shown to be restored with bilateral
stimulation [18], possibly acting as a ‘distractor’ to
reverse inhibition.
Previous studies have established the utility of specialized
electrophysiological techniques in aiding or confirming the
diagnosis of certain PMDs, particularly psychogenic tremor and psychogenic myoclonus. These studies have been
reviewed elsewhere [11,19,20]. Recent electrophysiological studies have better delineated PMDs. Compared with
controls, PMD patients exhibited an excessive affective
response to the startle eye blink reflex [21]. When pictures
invoking either positive or negative affective states were
shown at the time of eliciting the eye blink startle, reflex
potentiation was seen in both conditions, in contrast to the
normal inhibition with the negative affective state seen in
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432 Movement disorders
Table 2 Diagnostic classification of psychogenic movement disorders
Traditional
Proposed revision
Classification of degrees of certainty in diagnosisa
1. Documentedb
Remittance with suggestion, physiotherapy,
psychotherapy, placebos, ‘while unobserved’
2. Clinically establishedb
Inconsistent over time/incongruent with clinical
condition R other manifestations: other ‘false’
signs, multiple somatizations, obvious
psychiatric disturbance
3. Probable
Inconsistent/incongruent no other features
Consistent/congruent þ ‘false’ neurological signsc
Consistent/congruent þ multiple somatizationsc
4. Possibled
Consistent/congruent þ obvious emotional disturbancec
Classification of degrees of certainty in diagnosis
1. Documented (as in original)
2a. Clinically established plus other features (as in original)
2b. Clinically established minus other features
Unequivocal clinical features incompatible with organic
disease with no features suggesting another underlying
neurological or psychiatric problem
1 þ 2a þ 2b ¼ Clinically Definite
3. Laboratory-supported definite
Electrophysiological evidence proving a psychogenic
movement disorder (primarily in cases of psychogenic
tremor and psychogenic myoclonus)
a
Adapted from [12].
Subsequently, Fahn and his coauthors [10] proposed combining categories 1 þ 2 under ‘Clinically Definite’.
We proposed to reclassify these patients under ‘Possible’.
d
We also questioned the utility of retaining the ‘Possible’ category as this generally represents patients with organic movement disorders with
additional psychiatric problems rather than a true ‘Possible psychogenic movement disorder’ [11].
b
c
controls. It remains to be seen whether this result can
separate PMDs from organic disease, particularly in
patients with underlying concurrent psychopathology.
Central motor conduction is typically normal in patients
with MCD. Using transcranial magnetic stimulation
(TMS) in such patients, Liepert et al. [22] found that
motor threshold, short and long interval intracortical inhibition (SICI and LICI), and intracortical facilitation (ICF)
were similar to that in controls, indicating unchanged
baseline cortical excitability. When movements were imagined, however, cortical excitability was decreased in the
affected limb of MCD patients but increased in the
unaffected limb as it was in the limbs of healthy individuals. Further confirmatory studies are required. Theoretically, this decreased cortical excitability with motor imagery might be able to separate conversion disorder from
factitious disorder or malingering.
Some electrophysiological testing fails to distinguish
PMDs from organic movement disorders, indicating complex overlapping neuronal mechanisms and the importance of careful clinical assessment. Electrophysiological
findings are very similar between simulated propriospinal
myoclonus (PSM) and the organic counterpart [23]. Aside
from a generally longer electromyographic burst duration
observed in controls purposefully simulating PSM, a
fixed pattern of muscle recruitment, synchronous activation of agonist and antagonist, electromyographic burst
duration less than 1000 ms, and slow conduction in the
spinal cord (5–15 m/s) have been shown in both groups.
In a recent case of confirmed psychogenic PSM following
eye surgery [24], electrophysiological analysis demonstrated slow conduction, short burst duration, consistent
caudal muscle activation, and absence of premovement
potentials, with only some variability in muscle activation
possibly suggesting a PMD. Another example in which
PMDs and the organic counterpart may not be differentiated with electrophysiological studies is dystonia.
TMS has shown increased cortical excitability (decreased
SICI, LICI, ICF) in both groups [25], suggesting that this
abnormality can occur as a consequence of the dystonic
postures or, alternatively, it may be an ‘endophenotype’
that predisposes to the dystonia in both organic and
psychogenic cases. A distinction between these two
possibilities was not possible, as the unaffected side
was not investigated. Avanzino et al. [26] analyzed both
sides with TMS and obtained similar results, supporting
the conclusion that the cortical hyperexcitability may
reflect a predisposing ‘endophenotypic trait’ for dystonia
in either condition [27], although transcallosal or ipsilateral descending influences from the involved hemisphere
could still result in these changes being secondary to the
postures. Future investigation searching for improved
electrophysiological approaches could provide great
value, as clinical distinction between organic and psychogenic dystonia can be extremely challenging [28,29].
Posttraumatic movement disorders
Posttraumatic movement disorders are a source of considerable controversy. Complex regional pain syndrome
(CRPS) type I typically following minor injury may be
associated with fixed dystonia, myoclonus, and tremor.
Some authors have provided considerable evidence in
favor of a psychogenic cause [30,31], whereas others favor
an ‘organic’ explanation [32]. Munts et al. [33] recently
presented the electrophysiological characterization of
myoclonus associated with CRPS. However, it was subsequently argued that their findings of burst duration
length of more than 70 ms, variability in burst characteristics, side-to-side coherence, and entrainment were
strongly supportive of a psychogenic cause of the movements [34]. The ‘jumpy stump’ (an uncommon but widely
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Psychogenic movement disorders Gupta and Lang 433
acknowledged ‘peripheral’ movement disorder developing in an amputated limb) has been considered another
example of an organic posttraumatic movement disorder.
Zadikoff et al. [35] recently presented a case of psychogenic ‘jumpy stump’, in which paroxysmal rhythmical
jerking movements of the stump were associated with
palpable muscle activation in the proximal limb. Electrophysiological analysis confirmed reciprocal contraction
of hamstrings and quadriceps at 8 Hz, increased EMG
activity with stump restraint (indicating voluntary effort
against resistance), variability, and distractibility with
coherence. This case cautions against the uncritical application of the diagnosis of ‘jumpy stump’ as organic, but
the true prevalence of psychogenic movements in such
patients remains unclear without further systematic
study.
psychogenic tremor were diagnosed prior to assessment
of distinctive parameters, and sample size was small. In
addition, the method of evaluating entrainment (10 s of
wrist extension and flexion in the unaffected arm) is
probably not an adequate assessment of this feature.
Kumru et al. [42] assessed whether dual task interference
(difficulties with carrying out tasks simultaneously with
both arms) could distinguish psychogenic tremor from
Parkinsonian rest tremor and essential tremor. Only psychogenic tremor patients showed delayed reaction time
when they performed a simple reaction time task to a visual
stimulus with their nontremulous side when tremor was
present compared with when it was not. It is unclear
whether this method is superior to classic distraction
paradigms (with respect to ease of testing, reliability,
sensitivity, and specificity) and it requires that the tremor
be intermittent rather than persistent.
Psychogenic tremors
Psychogenic tremor can be remarkably variable in its
presentation, as supported by recent case reports [19],
as well as severe and disabling. Recent experience
suggests that the diagnosis should be considered in
patients failing deep brain stimulation surgery for tremor
[36]. In recent years, it has become clear that some patients
who would have been previously diagnosed as ‘essential
palatal tremor’ have a psychogenic cause. Recognizing the
heterogeneous nature of ‘essential palatal tremor’, including a PMD, a learned movement, and tics, Zadikoff et al.
[37] proposed the term ‘isolated palatal tremor’ to avoid
confusion with other more homogeneous disorders such as
essential tremor and essential myoclonus (now myoclonus
dystonia). Psychogenic palatal tremor may or may not have
extrapalatal movements. As in other forms of psychogenic
tremor, psychogenic palatal tremor is typically variable in
frequency (often changes in response to challenging motor
tasks), and it may be entrained and suppressed by distracting maneuvers. By definition, the MRI is always
normal [38]. One patient with a 2 Hz palatal tremor
restricted to the posterior soft palate determined to be
psychogenic even had a sensory trick that suppressed the
tremor [39]. Finally, psychogenic suprahyoid neck tremor
was recently reported; this appeared suddenly, was irregular, disappeared with open mouth or with distraction,
and resolved with placebo injection [40].
Investigations of how to better identify psychogenic tremor are ongoing. Kenney et al. [41] studied what features
might distinguish psychogenic tremor from essential tremor, given that sensitivity and specificity of psychogenic
clues generally lack systematic evaluation in this context.
Psychogenic tremor was differentiated by negative family
history, sudden onset, spontaneous remission, shorter
duration of tremor, suggestibility, and distractibility. Curiously, entrainment was not seen often in either tremor
type. The authors’ claim that the results have predictive
value is limited by the fact that essential tremor and
Evaluation of long-term prognosis of psychogenic tremor
has proven difficult, as underscored by two recent studies
with a similar follow-up period (3 years). Earlier investigations have reported tremor remission rates of only
20%. McKeon et al. [43] arrived at a similar pessimistic
outlook, finding a 65% disability rate on patient-reported
disability scales. In contrast, Jankovic et al. [44] reported a
better prognosis with a 60% improvement rate. However,
they included any degree of improvement, as measured
on a global rating scale, their patients had a shorter
duration of symptoms at the time of diagnosis (0.9 years
versus 1.5 years in the McKeon study), and they had a
greater proportion of patients enrolled in treatment. This
study also lacked a prospective follow-up design and
confirmatory electrophysiological assessment of psychogenic tremor used in the McKeon report. Nonetheless,
favorable prognostic signs were determined, which
included the patient’s perception of effective treatment
by the physician, elimination of stressors, and compliance
with the treatment regimen. No statistical difference in
long-term outcome was found between patients involved
and not involved in litigation.
Psychogenic gait disorders
Given the variable presentation of psychogenic gait [45],
formal tests definitively identifying this condition would
be very helpful but have yet to be developed. On the
basis of Paul Blocq’s original description of an astasia–
abasia patient who effectively propelled a chair while
being seated, Okun et al. [46] assessed whether this ‘chair
test’ could distinguish psychogenic from organic gait.
Eight of nine patients with psychogenic gait moved much
better sitting in a chair than when walking in the upright
position, whereas nine organic gait disorder patients
performed similarly in both conditions. Although promising, test sensitivity and specificity need to be assessed
with a larger sample size and a more diversified control
group (the control group had seven Parkinson’s disease
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
434 Movement disorders
patients); for example, patients with lower body dystonia
might show false positive results if they were able to use
the chair as a geste antagoniste, and patients with ‘gait
apraxia’ who can perform normal bicycling leg movements might also fair better in the chair than on standing.
Baik and Lang [47] assessed gait abnormalities in a large
group of patients with PMDs. When patients were
subdivided into those with more generalized PMDs
that also compromised the gait and those with a pure
psychogenic gait disorder, the mixed PMD group
most frequently showed slowness of gait (followed by
dystonic gait), whereas the pure gait group most commonly displayed buckling of knees (followed by astasia–
abasia). This study provides an incentive to assess
whether gait differences among PMD subpopulations
have diagnostic, predictive, or therapeutic value and
whether these differences reflect distinct pathophysiological processes.
Psychogenic movement disorders in children
PMDs in children have been addressed by recent reviews
[48,49]. Uncommon before the age of 10 years, clinical
clues in children are derived from the adult literature. As in
adults, there is female sex predominance, they comprise
approximately 3% of children visiting movement disorders
clinics, and the distribution of psychiatric diagnosis shows
conversion disorder in up to 80%, followed by somatization
disorders (10–20%) and factitious disorders (<5%). Quite
in contrast to the adults, malingering was not reported.
Similar to adults [10], dystonia and tremor were the most
common clinical phenotypes, followed remotely by gait
disorders. In addition, dystonia was fixed in most cases and
usually preceded by minor physical trauma.
Some differences are noteworthy. Although in adults the
nondominant limb may be most often affected (except for
tremor in psychogenic Parkinsonism), children more
frequently have PMDs in their dominant limb. It has
been suggested that this may reflect incomplete hemispheral lateralization [49]. Although coexisting organic
neurological disease is well recognized in patients with
psychogenic neurological complaints, associated organic
movement disorders are rare in children with PMDs [49]
in contrast to estimates in adults, which range between 10
and 25%. Similarly, psychiatric diseases in children
appear to be less common, as most studies report 10%
comorbidity, compared with the 40% rate quoted for
adults with PMDs. However, Ferrara and Jankovic
[48] reported a 50% comorbidity rate (anxiety, depression, irritability) and a 40% rate of perfectionistic personality, a common trait in patients with conversion disorders. Lastly, psychogenic dystonia is less easily and
comfortably diagnosed in children, given the spectrum
of organic dystonia that results from genetic mutations,
neurometabolic diseases, and other causes.
Treatment
A delay in diagnosing PMDs should be avoided at all
costs. Failure to do so often results in multiple referrals,
repeated unnecessary diagnostic tests, unjustified and
potentially harmful treatments including medication
trials and even surgeries, and the perpetuation of the
belief of underlying organic illness. This also delays the
initiation of appropriate treatment (though, as discussed
below, treatment is often very different), which reduces
efficacy, particularly if treatment is started 6–12 months
after onset of the movement disorder. To maximize
treatment compliance, it should be acknowledged that
the patient has a movement disorder (i.e. a form of
tremor, myoclonus, or dystonia) and a biological explanation provided. Lastly, despite the various treatments
applied, evidence-based data are limited, and prospective
double-blinded studies are urgently required.
Therapy is best administered in multimodal fashion.
Psychotherapy [50], cognitive behavioral therapy, rehabilitation [51,52], antidepressants [53], and hypnosis [54]
have had variable success. Monthly sessions of acupuncture produced normalization for only 4–5 days in a
patient with psychogenic jerking movements [55]. She
was wheelchair bound, with symptoms present for over a
decade. This effect may have simply been because of a
reduction of anxiety or some other form of placebo effect.
Recently, a 17-year-old boy with psychogenic aphonia for
20 months who had failed speech therapy recovered
completely following two sessions of repetitive TMS
[56]. Low-frequency stimulation was used, rather than
the high-frequency pulses usually applied to psychogenic
limb paralysis intended to directly activate the primary
motor areas. Functional imaging data in psychogenic
paralysis have shown decreased activity in the primary
motor cortex and increased activity in prefrontal cortex.
Thus, low-frequency stimulation may have inhibited the
overactive prefrontal areas resulting in disinhibition of
the primary motor cortex. Target choice might be critical;
low-frequency stimulation resulted in rapid recovery,
whereas high-frequency treatment takes many weeks
and produces variable success. In light of the strong
potential for a placebo effect, a controlled trial is clearly
needed to demonstrate reproducibility, taking into
account the well established effect of patient anticipation
on treatment outcomes [57].
Data on long-term prognosis are scarce, but most studies
point to significant impact on quality of life. Anderson
et al. [58] compared 66 patients with PMDs to 704 with
Parkinson’s disease and found increased psychiatric
comorbidity, more severe mental health disturbances,
and very similar levels of disability and physical quality
of life, despite the fact that patients with PMDs were
20 years younger, had shorter disease duration (4 versus
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Psychogenic movement disorders Gupta and Lang 435
7 years), and were compared to a Parkinson’s disease
population with a 30% prevalence of motor fluctuators.
Prognosis appears to be better in children with PMDs. In
one study [49], 50% of children remitted, 40% returned
to normal school life, whereas 20% experienced only
partial improvement or remained disabled. As with
adults, children who remitted were treated in their first
year after symptom onset, whereas those without
improvement had been symptomatic for many years
[49]. Remission was found to occur most often with
tremor, which may relate to early visits to the specialist,
whereas children with dystonia often did not improve.
Recent studies have shown that many children remain
disabled for several years; the long-term prognosis of
these children requires careful assessment.
5
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which criteria should be used in clinical practice? Nat Clin Pract Neurol 2007;
3:134–135.
6
Hinson VK, Haren WB. Psychogenic movement disorders. Lancet Neurol
2006; 5:695–700.
7
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Watts RL, Koller WC, editors. Movement disorders: neurologic principles and
practice. New York: McGraw Hill; 2004. pp. 891–914.
8
Pringsheim T, Chen R, Lang AE. Psychogenic movement disorders. In:
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9
Espay AJ, Fox SH, Marras C, et al. Isolated diaphragmatic tremor: is there a
spectrum in ‘respiratory myoclonus’? Neurology 2007; 69:689–692.
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Conclusion
PMDs can be diagnosed with reasonable certainty in
many cases, after limited ancillary testing is obtained.
Sometimes the diagnosis can be made with certainty on
the first clinical assessment and, at other times, comes
only after repeated careful evaluations and the exclusion
of other possible causes. The importance of special
electrophysiological analysis has been repeatedly emphasized, including in recent studies; however, availability of
expertise in this area may limit its broader application.
Critical is the realization that exclusively psychogenic or
organic findings may not always be available, but it is the
constellation and pattern of findings that leads to the
recognition of PMDs. Given the significant impact on
quality of life, future work should focus on assisting more
definitive early diagnosis, a better understanding of the
true pathogenesis of these disorders (including whether
there are unique differences or whether they are similar
to one another and to other somatoform disorders), and
finally on treatment trials that are tailored to providing
aggressive therapeutic intervention early on in the disease state and to patients with well established disabling
symptoms.
References and recommended reading
Papers of particular interest, published within the annual period of review, have
been highlighted as:
of special interest
of outstanding interest
Additional references related to this topic can also be found in the Current
World Literature section in this issue (p. 448).
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Perhaps surprisingly, though confirmation of a PMD was clinically not difficult
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Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
436 Movement disorders
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and long-term prognosis but also on similarities to and differences
from PMDs in the adult population. The comparison with adult PMDs is
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Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.