Elsevier

NeuroImage

Volume 47, Issue 3, September 2009, Pages 1015-1025
NeuroImage

Review
Psychogenic movement disorders: Aetiology, phenomenology, neuroanatomical correlates and therapeutic approaches

https://doi.org/10.1016/j.neuroimage.2009.04.082Get rights and content

Abstract

Paralysis and movement disorders unexplained by identifiable neurological disease are common clinical presentations in neurological outpatient clinics. Despite their frequency and potential importance from a neuroscientific viewpoint these disorders have received surprisingly little attention in clinically oriented neuroscientific research. In this review we summarize the available literature that specifically relates to the functional neuroanatomy of psychogenic movement disorders. We discuss the aetiology, clinical phenomenology, the current concepts of the dynamic neuroanatomical networks underlying psychogenic neurological syndromes as elucidated by neuroimaging and their potential implications for novel therapeutic approaches.

Introduction

Psychogenic neurological symptoms are deficits which cannot be explained by organic lesions in the nervous system and commonly are associated with emotional “functional” disturbances (Bhatia and Schneider, 2007, Hinson and Haren, 2006). Several terms, such as “functional”, “psychogenic”, “psychosomatic”, “non-organic”, “hysterical”, “conversion disorder” or “dissociative motor disorder” are used to describe neurological symptoms unexplained by disease (Mace and Trimble, 1991, Stone et al., 2002a, Stone et al., 2002b). The term “psychogenic” was first introduced into the literature by Robert Sommer, a German Psychiatrist, and has undergone several mutations since (Lewis, 1974). In the following we use the term “psychogenic” simply due to the fact that it appears to be the most widely used referring to movement disorders unexplained by organic disease. We do so being well aware of the fact that with the revision of the taxonomy used in the diagnostic and statistical manual for mental disorders (DSM-IV) the American Psychiatric Association (1994) abolished the functional–organic dichotomy. Psychogenic movement disorders are classified by the DSM-IV as conversion disorder of motor subtype.

Psychogenic neurological symptoms are common and account for 1–9% of neurological symptoms observed in the general population (Lempert et al., 1990, Factor et al., 1995). In principal, these symptoms can affect any aspect of neurological function. However, loss of movements (paralysis) or abnormal movements, such as tremor, are among the most common of psychogenic neurological disorders (Factor et al., 1995, Bhatia and Schneider, 2007). Psychogenic tremor (PT) and psychogenic paralysis (PP) due to conversion disorders of motor subtype must be differentiated from factitious disorder, and malingering. In factitious disorder symptoms are intentionally produced because of a psychological need as in Münchhausen's syndrome. In malingering symptoms are voluntarily produced to reach a certain goal, such as financial compensation or acquisition of drugs. In malingering the patient is lying to the physician.

In one series dividing medically unexplained motor symptoms into “absence of motor function” and “presence of abnormal motor activity”, 48% of the patients had index symptoms in the former category, while 52% had symptoms, such as tremor, dystonia or ataxia (Crimlisk et al., 1998). Psychogenic movement disorders account for about 2–3% of all patients seen in speciality clinics (Factor et al., 1995, Lang, 2006). Detailed epidemiological data are lacking, but population-based studies estimated the prevalence of PP and PT at approximately 2% (Rief et al., 2002, Jankovic and Thomas, 2006) and its incidence at about 5 per 100,000 (Binzer et al., 1997, Factor et al., 1995). Thus, the incidence of PP and PT is similar or even greater than that of other “organic” neurological disorders, such as multiple sclerosis (5 per 100,000) (Alonso and Hernan, 2008) or amyotrophic lateral sclerosis (1 per 100,000) (Abhinav et al., 2007).

Recently, one of the leading experts in the field of neurological movement disorders deemed psychogenic movement disorders as a “crisis for neurology” (Hallet, 2006). This opinion is based on (i) the significant number of patients presenting with psychogenic movement disorders, (ii) the lack of definitive clinical or laboratory tests to establish the diagnosis, (iii) the current lack of understanding about the exact nature of psychogenic movement disorders, (iv) poorly defined treatment options and (v) poor prognosis as physicians are frequently reluctant to make the diagnosis with the patients being commonly resistant to both diagnosis and therapeutic interventions. Although current concepts tend to explain psychogenic movement disorders in the context of “psychogenic stress” or “emotional disturbances” recent functional neuroimaging studies have started to shift our understanding of these deficits from a psychological and psychodynamic model to a neurobiological model (Montoya et al., 2006, Vuilleumier, 2005, Vuilleumier et al., 2001). To date it remains unclear whether or not this may also allow for a development of novel concepts for both diagnosis and therapy of PP and PT. This review summarizes data regarding aetiology, clinical presentation and diagnostic pathways, while putting particular emphasize on our current understanding of the neural correlates and novel therapeutic approaches in patients suffering from PP and PT.

Section snippets

Theories on aetiology

Over more than a century of both clinical and theoretical interest there is a large body of literature regarding the possible psychogenic, psychoanalytical, cultural and biological mechanisms underlying psychogenic movement disorders (Reynolds, 1869, Charcot, 1889). The fundamental problem with such general approaches is that they make the assumption that all patients presenting with neurological symptoms unexplained by “organic” disease suffer from the same disorder, which is unlikely to be

Demographics, psychiatric co-morbidity and outcome

PP is observed over a wide range of ages from childhood to the mid seventies (Zhang et al., 1987). The average age at onset is in the mid thirties (Teasell and Shapiro, 1997, Ziv et al., 1998, Zhang et al., 1987). The available literature does report either no gender predominance (Binzer et al., 1997, Cantello et al., 2001) or a slight female predominance in PP (Zhang et al., 1987). In the only prospective case control study currently available, Binzer et al., 1997, Binzer et al., 1998)

Diagnostic clues

The diagnosis of PP and PT should be based on positive clinical criteria, the presence of which should prevent unnecessary investigation (Jankovic and Thomas, 2006, Stone et al., 2007). The huge majority of PP and PT have an abrupt onset (Binzer et al., 1997, Binzer et al., 1998, Deuschl et al., 1998, Kim et al., 1999, Koller et al., 1989). A thorough (psychiatric) exploration should explore childhood history, personality factors, psychiatric history, drug experience, recent personal and family

Treatment

PT and PP affects mainly people under retirement age and is therefore associated with substantial health-care costs (Margalit and El-Ad, 2008). Treatment regimen for PT and PP include placebo therapy, antidepressant medication, psychotherapy, psychological therapy, biofeedback, physical and occupational therapy (Aybek et al., 2008, Jankovic et al., 2006, Williams et al., 1995). However, there are no larger controlled trials allowing definitive judgement about the effectiveness of any of these

Neural correlates

Within recent years several functional brain imaging techniques, such as functional magnetic resonance imaging (fMRI), positron emission tomography (PET) and single photon emission computed tomography (SPECT) were used in an attempt to identify specific neural correlates associated with medically unexplained loss of motor function or parkinsonism. It should be mentioned that no neuroimaging study was designed to specifically explain the dissociation process per se nor how the conversion process

Functional neuroimaging in psychogenic paralysis

Functional neuroimaging has revealed selective decreases in the neural activity of frontal and subcortical motor circuits in PP (De Lange et al., 2007, Fink et al., 2006, Marshall et al., 2002, Tiihonen et al., 1995, Yaici and Kostakoglu, 1998, Vuilleumier et al., 2001). Such changes are usually not accompanied by any significant changes in elementary stages of sensory or motor processing as assessed by neurophysiology, such as somatosensory or motor evoked potentials (Pillai et al., 1992,

Functional neuroimaging in psychogenic tremor

PET or fMRI data in PT do not exist. The role of the striatal dopamine transporter/dopamine uptake imaging in patients with parkinsonism is still a matter of debate (Benaderette et al., 2006, Eerola et al., 2005, Marshall and Grosset, 2003). [123I]β-CIT striatal dopamine transporter imaging (Eerola et al., 2005) and striatal [18F]DOPA uptake imaging (Poewe and Scherfler, 2003) are helpful to distinguish patients with parkinsonian syndromes, such as drug-induced parkinonism, Parkinson-plus

Novel treatment approaches based on neuroimaging data

Repetitive transcranial magnetic stimulation (rTMS) can change cortical excitability depending on the rate and intensity of stimulation (Pascual-Leone et al., 1994). Schönfeldt-Lecuona et al. (2006) treated four patients with PP over a period of 5–12 weeks with a facilitatory rTMS protocol (stimulation frequency: 15 Hz, train length: 2 s, inter-train interval: 4 s; daily total number of stimuli 4000) increasing cortical excitability of the contralateral motor cortex. One patient recovered

Conclusion and future research directions

Paralysis and tremor unexplained by identifiable neurological disease are common clinical presentations in neurological outpatient clinics. Despite their frequency and potential importance from a neuroscientific viewpoint these disorders have received surprisingly little attention in clinically oriented neuroscientific research. Despite discrepancies within the pertinent literature, the most convincing theory is presently based on active inhibition of motor areas by limbic brain areas in PP. On

Acknowledgments

We would like to thank Floris De Lange at the Donders Institute for Brain, Cognition and Behaviour in Nijmegen, the Netherlands, for providing Fig. 2, Fig. 3. The present work was supported by a grant of the Deutsche Forschungsgemeinschaft to Dennis A. Nowak (NO 737/4-1).

References (86)

  • SpenceS.A. et al.

    Discrete neurophysiological correlates in prefrontal cortex during hysterical and feigned disorder of movement

    Lancet

    (2000)
  • von GiesenHJ et al.

    Cerebral network underlying unilateral motor neglect: evidence from positron emission tomography

    J. Neurol. Sci.

    (1994)
  • VuilleumierP.

    Hysterical conversion and brain function

    Prog. Brain Res.

    (2005)
  • AbhinavK. et al.

    Amyotrophic lateral sclerosis in South-East England: a population-based study. The South-East England register for amyotrophic lateral sclerosis (SEALS Registry)

    Neuroepidemiology

    (2007)
  • AlonsoA. et al.

    Temporal trends in the incidence of multiple sclerosis: a systematic review

    Neurology

    (2008)
  • Diagnostic and Statistical Manual for Mental Disorders

    (1994)
  • AybekS. et al.

    The neuropsychiatry of conversion disorder

    Curr. Opin. Psychiatry

    (2008)
  • BeardG.

    Experiments with the “jumpers” or “jumping Frenchmen” of Maine

    J. Nerv. Ment. Dis.

    (1880)
  • BenaderetteS. et al.

    Psychogenic parkinsonism: a combination of clinical, electrophysiological, and [(123)I]-FP-CIT SPECT scan explorations improves diagnostic accuracy

    Mov. Disord.

    (2006)
  • BhatiaK.P. et al.

    Psychogenic tremor and related disorders

    J. Neurol.

    (2007)
  • BinzerM. et al.

    Clinical characteristics of patients with motor disability due to conversion disorder: a prospective control group study

    J. Neurol. Neurosurg. Psychiatry

    (1997)
  • BlissE.L.

    Hysteria and hypnosis

    J. Nerve Ment. Disord.

    (1984)
  • CantelloR. et al.

    Diagnosis of psychogenic paralysis: the role of motor evoked potentials

    J. Neurol.

    (2001)
  • CharcotJ.M.
  • ChladerT.

    Cognitive behavioural therapy as a treatment for conversion disorder

  • CrimliskH.L. et al.

    Slater revisited: 6 year follow up study of patients with medically unexplained motor symptoms

    Br. Med. J.

    (1998)
  • DafotakisM. et al.

    Psychogenic tremor

    Fortschr. Neurol. Psychiatr.

    (2008)
  • DeuschlG. et al.

    Diagnostic and pathophysiological aspects of psychogenic tremors

    Mov. Disord.

    (1998)
  • EerolaJ. et al.

    How useful is [123I]beta-CIT SPECT in clinical practice?

    J. Neurol. Neurosurg. Psychiatry

    (2005)
  • FactorS.A. et al.

    Psychogenic movement disorders. Frequency, clinical profile and characteristics

    J. Neurol. Neurosurg. Psychiatry

    (1995)
  • FactorS.A. et al.

    Psychogenic parkinsonism: confirmation of diagnosis with β-CIT SPECT scans

    Mov. Disord.

    (1998)
  • FahnS. et al.

    Psychogenic dystonia

    Adv. Neurol.

    (1988)
  • FeinsteinA. et al.

    Psychiatric outcome in patients with a psychogenic movement disorder: a prospective study

    Neuropsychiatry Neuropsychol. Behav. Neurol.

    (2001)
  • FinkG.R. et al.

    Neuroimaging of hysteria

  • FreudS.

    Psycho-analytic view of psychogenic disturbance of vision

  • HalletM.

    Psychogenic movement disorders: a crisis for neurology

    Curr. Neurol. Neurosci. Rep.

    (2006)
  • HammondW.A.
  • HooverC.F.

    A new sign fort he detection of malingering and functional paraesis of the lower extremities

    JAMA

    (1908)
  • JankovicJ. et al.

    Therapeutic approaches to psychogenic movement disorders

  • JankovicJ. et al.

    Psychogenic tremor and shaking

  • JenningsD.L. et al.

    (123I) beta-CIT and single-photon emission computed tomographic imaging vs clinical evaluation in Parkinsonian syndrome: unmasking an early diagnosis

    Arch. Neurol.

    (2004)
  • KhalilT.M. et al.

    Functional electric stimulation in the renewal of conversion disorder paralysis

    Arch. Phys. Med. Rehab.

    (1988)
  • KimY.J. et al.

    Historical and clinical features of psychogenic tremor: a review of 70 cases

    Can. J. Neurol. Sci.

    (1999)
  • Cited by (57)

    • Ictal SPECT in Psychogenic Nonepileptic and Epileptic Seizures

      2021, Journal of the Academy of Consultation-Liaison Psychiatry
      Citation Excerpt :

      Despite being routinely chosen as a method to investigate PNES in several epilepsy centers worldwide,26,27 provocative tests similar to the one we used might influence brain metabolism.28–30 However, it must also be considered that, since the first functional neurological symptoms study, suggestibility and hypnotizability are conceptualized as an integral part of the cognitive process involving dissociation and conversion.31 Study strengths are underscored.

    • Impaired emotion processing in functional (psychogenic) tremor: A functional magnetic resonance imaging study

      2018, NeuroImage: Clinical
      Citation Excerpt :

      Despite its frequency and the magnitude of disability it imparts, the pathophysiological underpinnings of FT remain poorly understood and no effective treatments have been established. Neuroimaging studies have suggested that the basal ganglia and limbic systems are integral parts of the neural pathways for processing emotions (Nowak and Fink, 2009). Recent functional neuroimaging studies of patients with functional movement disorders have demonstrated alterations in regional cerebral blood flow during simple motor tasks (Schrag et al., 2013) or in brain activation of the cerebellar vermis, posterior cingulate cortex, and hippocampus on isometric precision-grip contraction tasks (Blakemore et al., 2016) as well as in brain activation of the right amygdala on simple emotional stimuli (n = 10) (Voon et al., 2010) or both amygdala on stimulation on fearful emotional stimuli (n = 12) (Aybek et al., 2015).

    View all citing articles on Scopus
    View full text