Top

Current Neurology and Neuroscience Reports

Published in:

Open Access 01-11-2013 | Neuroimaging (DJ Brooks, Section Editor)

Imaging Psychogenic Movement Disorders

Authors: Arpan R. Mehta, James B. Rowe, Anette E. Schrag

Published in: Current Neurology and Neuroscience Reports | Issue 11/2013

Abstract

The neurobiological basis of psychogenic movement disorders (PMDs) has been elusive, and they remain difficult to treat. In the last few years, functional neuroimaging studies have provided insight into their pathophysiology and neural correlates. Here, we review the various methodological approaches that have been used in both clinical and research practice to address neural correlates of functional disorders. We then review the dominant hypotheses generated from the literature on psychogenic paralysis. Overall, these studies emphasize abnormalities in the prefrontal and anterior cingulate cortices. Recently, functional neuroimaging has been used to specifically examine PMDs. These studies have addressed a major point of controversy: whether higher frontal brain areas are directly responsible for inhibiting motor areas or whether they reflect modulation by attentional and/or emotional processes. In addition to elucidating the mechanism and cause, recent work has also explored the lack of agency that characterizes PMDs. We describe the results and implications of the results of these imaging studies and discuss possible interpretations.

Edwards MJ, Bhatia KP. Functional (psychogenic) movement disorders: merging mind and brain. Lancet Neurol. 2012;11(3):250–260. doi:10.1016/S1474-4422(11)70310-6.

Nowak DA, Fink GR. Psychogenic movement disorders: aetiology, phenomenology, neuroanatomical correlates and therapeutic approaches. Neuroimage. 2009;47(3):1015–1025. doi:10.1016/j.neuroimage.2009.04.082.

Ellenstein A, Kranick SM, Hallett M. An update on psychogenic movement disorders. Curr Neurol Neurosci Rep. 2011;11(4):396–403. doi:10.1007/s11910-011-0205-z.

Lang AE, Voon V. Psychogenic movement disorders: past developments, current status, and future directions. Mov Disord. 2011;26(6):1175–1186. doi:10.1002/mds.23571.

Batshaw ML, Wachtel RC, Deckel AW, et al. Munchausen's syndrome simulating torsion dystonia. N Engl J Med. 1985;312(22):1437–1439. doi:10.1056/NEJM198505303122207.

Hallett M. Psychogenic movement disorders: a crisis for neurology. Curr Neurol Neurosci Rep. 2006;6(4):269–271.

Williams DT, Ford B, Fahn S. Phenomenology and psychopathology related to psychogenic movement disorders. Adv Neurol. 1995;65:231–257.

Factor SA, Podskalny GD, Molho ES. Psychogenic movement disorders: Frequency, clinical profile, and characteristics. J Neurol Neurosurg Psychiatry. 1995;59(4):406–412.

Stone J, Carson A, Duncan R, et al. Who is referred to neurology clinics?--the diagnoses made in 3781 new patients. Clin Neurol Neurosurg. 2010;112(9):747–751. doi:10.1016/j.clineuro.2010.05.011.

10.

Kranick SM, Gorrindo T, Hallett M. Psychogenic movement disorders and motor conversion: a roadmap for collaboration between neurology and psychiatry. Psychosomatics. 2011;52(2):109–116. doi:10.1016/j.psym.2010.12.017.

11.

Morgante F, Edwards MJ, Espay AJ, et al. Diagnostic agreement in patients with psychogenic movement disorders. Mov Disord. 2012;27(4):548–552. doi:10.1002/mds.24903.

12.

Schrag A, Trimble M, Quinn N, et al. The syndrome of fixed dystonia: an evaluation of 103 patients. Brain. 2004;127(10):2360–2372. doi:10.1093/brain/awh262.

13.

van Rijn MA, Munts AG, Marinus J, et al. Intrathecal baclofen for dystonia of complex regional pain syndrome. Pain 2009;143(1–2):41–47. doi:10.1016/j.pain.2009.01.014.

14.

Shamy MC. The treatment of psychogenic movement disorders with suggestion is ethically justified. Mov Disord. 2010;25(3):260–264. doi:10.1002/mds.22911.

15.

Edwards MJ, Alonso-Canovas A, Schrag A, et al. Limb amputations in fixed dystonia: a form of body integrity identity disorder? Mov Disord. 2011;26(8):1410–1414. doi:10.1002/mds.23671.

16.

Stone J, Sharpe M, Rothwell PM, et al. The 12 year prognosis of unilateral functional weakness and sensory disturbance. J Neurol Neurosurg Psychiatry. 2003;74(5):591–596.

17.

Jankovic J, Vuong KD, Thomas M. Psychogenic tremor: long-term outcome. CNS Spectr 2006;11(7):501–508.

18.

Thomas M, Vuong KD, Jankovic J. Long-term prognosis of patients with psychogenic movement disorders. Parkinsonism Relat Disord. 2006;12(6):382–387. doi:10.1016/j.parkreldis.2006.03.005.

19.

Carson A, Stone J, Hibberd C, et al. Disability, distress and unemployment in neurology outpatients with symptoms 'unexplained by organic disease'. J Neurol Neurosurg Psychiatry. 2011;82(7):810–813. doi:10.1136/jnnp.2010.220640.

20.

Kanaan RA, Armstrong D, Wessely SC. Neurologists' understanding and management of conversion disorder. J Neurol Neurosurg Psychiatry. 2011;82(9):961–966. doi:10.1136/jnnp.2010.233114.

21.

Espay AJ, Goldenhar LM, Voon V, et al. Opinions and clinical practices related to diagnosing and managing patients with psychogenic movement disorders: An international survey of movement disorder society members. Mov Disord 2009;24(9):1366–1374. doi:10.1002/mds.22618.

22.

Browning M, Fletcher P, Sharpe M. Can neuroimaging help us to understand and classify somatoform disorders? A systematic and critical review. Psychosom Med. 2011;73(2):173–184. doi:10.1097/PSY.0b013e31820824f6.

23.

Atmaca M, Aydin A, Tezcan E, et al. Volumetric investigation of brain regions in patients with conversion disorder. Prog Neuropsychopharmacol Biol Psychiatry. 2006;30(4):708–713. doi:10.1016/j.pnpbp.2006.01.011.

24.

Kagi G, Bhatia KP, Tolosa E. The role of DAT-SPECT in movement disorders. J Neurol Neurosurg Psychiatry 2010;81(1):5–12. doi:10.1136/jnnp.2008.157370.

25.

Felicio AC, Shih MC, Godeiro-Junior C, et al. Molecular imaging studies in Parkinson disease: reducing diagnostic uncertainty. Neurologist. 2009;15(1):6–16. doi:10.1097/NRL.0b013e318183fdd8.

26.

Marek K, Jennings D, Seibyl J. Imaging the dopamine system to assess disease-modifying drugs: studies comparing dopamine agonists and levodopa. Neurology. 2003;61(6 Suppl 3):S 43–48.

27.

Parkinson Study Group. A randomized controlled trial comparing pramipexole with levodopa in early Parkinson's disease: design and methods of the CALM-PD study. Clin Neuropharmacol. 2000;23(1):34–44.

28.

Whone AL, Watts RL, Stoessl AJ, et al. Slower progression of Parkinson's disease with ropinirole versus levodopa: the REAL-PET study. Ann Neurol. 2003;54(1):93–101. doi:10.1002/ana.10609.

29.

Hallett M, Rothwell J. Milestones in clinical neurophysiology. Mov Disord 2011;26(6):958–967. doi:10.1002/mds.23572.

30.

Friston KJ, Buechel C, Fink GR, et al. Psychophysiological and modulatory interactions in neuroimaging. Neuroimage. 1997;6(3):218–229. doi:10.1006/nimg.1997.0291.

31.

Roebroeck A, Formisano E, Goebel R. The identification of interacting networks in the brain using fMRI: Model selection, causality and deconvolution. Neuroimage. 2011;58(2):296–302. doi:10.1016/j.neuroimage.2009.09.036.

32.

Friston K, Moran R, Seth AK. Analysing connectivity with Granger causality and dynamic causal modelling. Curr Opin Neurobiol, 2013;23(2):172–178. doi:10.1016/j.conb.2012.11.010.

33.

Edwards MJ, Moretto G, Schwingenschuh P, et al. Abnormal sense of intention preceding voluntary movement in patients with psychogenic tremor. Neuropsychologia. 2011;49(9):2791–2793. doi:10.1016/j.neuropsychologia.2011.05.021.

34.

Kranick SM, Moore JW, Yusuf N, et al. Action-effect binding is decreased in motor conversion disorder: implications for sense of agency. Mov Disord. 2013;28(8):1110–1116. doi:10.1002/mds.25408.

35.

Parees I, Saifee TA, Kassavetis P, et al. Believing is perceiving: mismatch between self-report and actigraphy in psychogenic tremor. Brain. 2012;135(1):117–123. doi:10.1093/brain/awr292.

36.

Parees I, Kassavetis P, Saifee TA, et al. 'Jumping to conclusions' bias in functional movement disorders. J Neurol Neurosurg Psychiatry. 2012;83(4):460–463. doi:10.1136/jnnp-2011-300982.

37.

Morgante F, Tinazzi M, Squintani G, et al. Abnormal tactile temporal discrimination in psychogenic dystonia. Neurology. 2011;77(12):1191–1197. doi:10.1212/WNL.0b013e31822f0449.

38.

Mehta AR, Rowe JB, Trimble MR, et al. Coactivation sign in fixed dystonia. Parkinsonism Relat Disord. 2013;19(4):474–476. doi:10.1016/j.parkreldis.2012.10.014.

39.

Schwingenschuh P, Katschnig P, Seiler S, et al. Moving toward "laboratory-supported" criteria for psychogenic tremor. Mov Disord. 2011;26(14);2509–2515. doi:10.1002/mds.23922.

40.

Deuschl G, Köster B, Lücking CH, et al. Diagnostic and pathophysiological aspects of psychogenic tremors. Mov Disord. 1998;13(2):294–302. doi:10.1002/mds.870130216.

41.

Tiihonen J, Kuikka J, Viinamaki H, et al. Altered cerebral blood flow during hysterical paresthesia. Biol Psychiatry. 1995;37(2):134–135. doi:10.1016/0006-3223(94)00230-Z.

42.

Marshall JC, Halligan PW, Fink GR, et al. The functional anatomy of a hysterical paralysis. Cognition. 1997;64(1):B1–8.

43.

Yazici KM, Kostakoglu L. Cerebral blood flow changes in patients with conversion disorder. Psychiatry Res. 1998;83(3):163–168.

44.

Spence SA, Crimlisk HL, Cope H, et al. Discrete neurophysiological correlates in prefrontal cortex during hysterical and feigned disorder of movement. Lancet 2000;355(9211):1243–1244. doi:10.1016/S0140-6736(00)02096-1.

45.

Vuilleumier P, Chicherio C, Assal F, et al. Functional neuroanatomical correlates of hysterical sensorimotor loss. Brain. 2001;124(6):1077–1090.

46.

Mailis-Gagnon A, Giannoylis I, Downar J, et al. Altered central somatosensory processing in chronic pain patients with "hysterical" anesthesia. Neurology. 2003;60(9):1501–1507.

47.

Werring DJ, Weston L, Bullmore ET, et al. Functional magnetic resonance imaging of the cerebral response to visual stimulation in medically unexplained visual loss. Psychol Med. 2004;34(4):583–589. doi:10.1017/S0033291703008985.

48.

Burgmer M, Konrad C, Jansen A, et al. Abnormal brain activation during movement observation in patients with conversion paralysis. Neuroimage. 2006;29(4):1336–1343. doi:10.1016/j.neuroimage.2005.08.033.

49.

Ghaffar O, Staines WR, Feinstein A. Unexplained neurologic symptoms: an fMRI study of sensory conversion disorder. Neurology. 2006;67(11):2036–2038. doi:10.1212/01.wnl.0000247275.68402.fc.

50.

de Lange FP, Roelofs K, Toni I. Increased self-monitoring during imagined movements in conversion paralysis. Neuropsychologia. 2007;45(9):2051–2058. doi:10.1016/j.neuropsychologia.2007.02.002.

51.

Kanaan RA, Craig TK, Wessely SC, et al. Imaging repressed memories in motor conversion disorder. Psychosom Med. 2007;69(2):202–205. doi:10.1097/PSY.0b013e31802e4297.

52.

Stone J, Zeman A, Simonotto E, et al. FMRI in patients with motor conversion symptoms and controls with simulated weakness. Psychosom Med. 2007;69(9):961–969. doi:10.1097/PSY.0b013e31815b6c14.

53.

Cojan Y, Waber L, Carruzzo A, et al. Motor inhibition in hysterical conversion paralysis. Neuroimage. 2009;47(3):1026–1037. doi:10.1016/j.neuroimage.2009.05.023.

54.

de Lange FP, Toni I, Roelofs K. Altered connectivity between prefrontal and sensorimotor cortex in conversion paralysis. Neuropsychologia. 2010;48(6):1782–1788. doi:10.1016/j.neuropsychologia.2010.02.029.

55.

• Voon V, Gallea C, Hattori N, et al. The involuntary nature of conversion disorder. Neurology. 2010;74(3):223–228. doi:10.1212/WNL.0b013e3181ca00e9. Psychogenic tremor was associated with right temporoparietal junction hypoactivity and lower interactions between this area and the sensorimotor cortex. The right temporoparietal junction is thought to be an important comparator region, comparing actual with predicted sensory feedback. The absence of a feedforward signal would lead to a mismatch in the temporoparietal junction, such that the actual feedback would be received 'unchecked', owing to a lack of predicted sensory feedback (corollary discharge). This is hypothesized to provoke the feeling of involuntariness associated with movement: a lack of agency.

56.

• Voon V, Brezing C, Gallea C, et al. Emotional stimuli and motor conversion disorder. Brain. 2010;133(5):1526–1536. doi:10.1093/brain/awq054. This study demonstrated abnormally strong amygdala–supplementary motor area connectivity when patients with PMDs were presented with emotionally valent stimuli. The heightened amygdala activity to arousal is hypothesized to have downstream effects on motor initiation and nonconscious response inhibition.

57.

• Voon V, Brezing C, Gallea C, et al. Aberrant supplementary motor complex and limbic activity during motor preparation in motor conversion disorder. Mov Disord. 2011;26(13):2396–2403. doi:10.1002/mds.23890. This study showed reduced activity in the supplementary motor area in PMDs and increased activity in the amygdala and other areas implicated in emotional salience. It also showed reduced functional connectivity between the supplementary motor area and bilateral prefrontal cortices for internally generated movements. This is hypothesized to account for a potential impairment in top-down regulation of motor control to guide action selection.

58.

Czarnecki K, Jones DT, Burnett MS, et al. SPECT perfusion patterns distinguish psychogenic from essential tremor. Parkinsonism Relat Disord. 2011;17(5):328–332. doi:10.1016/j.parkreldis.2011.01.012.

59.

Hedera P. Metabolic hyperactivity of the medial posterior parietal lobes in psychogenic tremor. Tremor Other Hyperkinet Mov (N Y) 2012;2:tre-02-50-441-1.

60.

• Schrag AE, Mehta AR, Bhatia KP, et al. The functional neuroimaging correlates of psychogenic versus organic dystonia. Brain. 2013;136(3):770–781. doi:10.1093/brain/awt008. This article demonstrated a subcortical–cortical differentiation between organic (DYT1 gene mutation positive) and psychogenic (fixed) dystonia in terms of regional cerebral perfusion, with the latter patient group being characterized by abnormally increased perfusion in the cerebellum and basal ganglia, and abnormally decreased perfusion in the primary motor cortex (medial leg area); the opposite pattern was demonstrated in organic dystonia. The celebrated classic finding of abnormal prefrontal cortical activation in psychogenic neurological disorders was shown to not be exclusive to the psychogenic cause, because it was also seen in the organic dystonia group. The authors suggest that derangements in the mechanisms of motor attention may be a feature common to both conditions.

61.

• Edwards MJ, Adams RA, Brown H, et al. A Bayesian account of 'hysteria'. Brain. 2012;135(11):3495–3512. doi:10.1093/brain/aws129. This article provides a cogent account invoking a Bayesian hierarchical model to explain functional motor and sensory symptoms—they are pathologically precise prior beliefs modulated by attentional processes, resulting in perceptual and/or motor symptoms (posterior beliefs) that are experienced by the patient as being involuntary.

62.

Rowe JB. Conversion disorder: understanding the pathogenic links between emotion and motor systems in the brain. Brain. 2010;133(5):1295–1297. doi:10.1093/brain/awq096.

63.

Halligan PW, Athwal BS, Oakley DA, et al. Imaging hypnotic paralysis: implications for conversion hysteria. Lancet. 2000;355(9208):986–987. doi:10.1016/S0140-6736(00)99019-6.

64.

Ward NS, Oakley DA, Frackowiak RS, et al. Differential brain activations during intentionally simulated and subjectively experienced paralysis. Cogn Neuropsychiatry. 2003;8(4):295–312. doi:10.1080/13546800344000200.

65.

Roelofs K, van Galen GP, Keijsers GP, et al. Motor initiation and execution in patients with conversion paralysis. Acta Psychol (Amst). 2002;110(1):21–34.

66.

Roelofs K, de Bruijn ERA, Van Galen GP. Hyperactive action monitoring during motor-initiation in conversion paralysis: an event-related potential study. Biol Psychol 2006;71(3):316–325. doi:10.1016/j.biopsycho.2005.07.002.

67.

de Lange FP, Roelofs K, Toni I. Motor imagery: a window into the mechanisms and alterations of the motor system. Cortex. 2008;44(5):494–506. doi:10.1016/j.cortex.2007.09.002.

68.

Vuilleumier P. The neurophysiology of self-awareness disorders in conversion hysteria. In: Laureys S, Tononi G, editors. The neurology of consciousness: cognitive neuroscience and neuropathology. Amsterdam: Academic; 2009. p. 282–302.CrossRef

69.

Burgess PW, Dumontheil I, Gilbert SJ. The gateway hypothesis of rostral prefrontal cortex (area 10) function. Trends Cogn Sci. 2007;11(7):290–298. doi:10.1016/j.tics.2007.05.004.

70.

Bhatia KP, Schneider SA. Psychogenic tremor and related disorders. J Neurol. 2007;254(5):569–574. doi:10.1007/s00415-006-0348-z.

71.

Hallett M, Fahn S, Jankovic J, et al., editors. Psychogenic movement disorders: neurology and neuropsychiatry. Philadelphia: Lippincott Williams & Wilkins; 2005.

72.

Krem MM. Motor conversion disorders reviewed from a neuropsychiatric perspective. J Clin Psychiatry. 2004;65(6):783–790.

73.

Bogousslavsky J. Hysteria after Charcot: back to the future. Front Neurol Neurosci. 2011;29:137–161. doi:10.1159/000321783.

74.

Seignourel PJ, Miller K, Kellison I, et al. Abnormal affective startle modulation in individuals with psychogenical movement disorder. Mov Disord. 2007;22(9):1265–1271. doi:10.1002/mds.21451.

75.

Horvath T, Friedman J, Meares R. Attention in hysteria: a study of Janet's hypothesis by means of habituation and arousal measures. Am J Psychiatry. 1980;137(2):217–220.

76.

Lader M, Sartorius N. Anxiety in patients with hysterical conversion symptoms. J Neurol Neurosurg Psychiatry. 1968;31(5):490–495.

77.

Hallett M. Physiology of psychogenic movement disorders. J Clin Neurosci. 2010;17(8):959–965. doi:10.1016/j.jocn.2009.11.021.

78.

Shibasaki H, Hallett M. What is the Bereitschaftspotential? Clin Neurophysiol. 2006;117(11):2341–2356. doi:10.1016/j.clinph.2006.04.025.

79.

Farrer C, Frith CD. Experiencing oneself vs another person as being the cause of an action: the neural correlates of the experience of agency. Neuroimage. 2002;15(3):591–603. doi:10.1006/nimg.2001.1009.

80.

Blakemore SJ, Sirigu A. Action prediction in the cerebellum and in the parietal lobe. Exp Brain Res. 2003;153(2):239–245. doi:10.1007/s00221-003-1597-z.

81.

Schnell K, Heekeren K, Daumann J, et al. Correlation of passivity symptoms and dysfunctional visuomotor action monitoring in psychosis. Brain. 2008;131(10):2783–2797. doi:10.1093/brain/awn184.

82.

Ibrahim NM, Martino D, van de Warrenburg BP, et al. The prognosis of fixed dystonia: a follow-up study. Parkinsonism Relat Disord. 2009;15(8):592–597. doi:10.1016/j.parkreldis.2009.02.010.

83.

Quartarone A, Rizzo V, Terranova C, et al. Abnormal sensorimotor plasticity in organic but not in psychogenic dystonia. Brain. 2009;132(10):2871–2877. doi:10.1093/brain/awp213.

84.

Rowe JB, Siebner HR. The motor system and its disorders. Neuroimage. 2012;61(2):464–477. doi:10.1016/j.neuroimage.2011.12.042.

85.

Groenewegen HJ, Wright CI, Uylings HB. The anatomical relationships of the prefrontal cortex with limbic structures and the basal ganglia. J Psychopharmacol. 1997;11(2):99–106.

86.

Pollak TA, Nicholson TR, Edwards MJ, et al. A systematic review of transcranial magnetic stimulation in the treatment of functional (conversion) neurological symptoms. J Neurol Neurosurg Psychiatry. 2013. doi:10.1136/jnnp-2012-304181.

Title: Imaging Psychogenic Movement Disorders
Authors: Arpan R. Mehta
James B. Rowe
Anette E. Schrag
Publication date: 01-11-2013
Publisher: Springer US
Published in: Current Neurology and Neuroscience Reports / Issue 11/2013
Print ISSN: 1528-4042
Electronic ISSN: 1534-6293
DOI: https://doi.org/10.1007/s11910-013-0402-z

Keynote webinar | Spotlight on medication adherence

Springer Medicine

Imaging Psychogenic Movement Disorders

Abstract

Keynote webinar | Spotlight on medication adherence

Springer Medicine

Abstract

Please log in to get access to this content

Other articles of this Issue 11/2013

Towards a Clearer Definition of Logopenic Progressive Aphasia

Spinocerebellar Ataxia Type 10: From Amerindians to Latin Americans

Iatrogenic Fungal Infections of Central Nervous System

Monoclonal Antibodies as Disease Modifying Therapy in Multiple Sclerosis

The Evolving Role of Diffusion Magnetic Resonance Imaging in Movement Disorders

Neuro-Ophthalmic Deficits after Head Trauma