Hostname: page-component-76fb5796d-skm99 Total loading time: 0 Render date: 2024-04-25T15:39:59.089Z Has data issue: false hasContentIssue false

Abnormal gait and bradykinesia in the preclinical phase of Huntington's disease – psychogenic movement disorder?

Published online by Cambridge University Press:  24 June 2014

Witold Soltan
Affiliation:
Department of Neurology, St. Adalbert Hospital, Gdansk, Poland
Emilia Sitek
Affiliation:
Department of Neurology, St. Adalbert Hospital, Gdansk, Poland Department of Psychiatric- Neurological Nursing, Medical University of Gdansk, Gdansk, Poland
Hubert Wichowicz
Affiliation:
Department of Psychiatry, Medical University of Gdansk, Gdansk, Poland
Dariusz Wieczorek
Affiliation:
Department of Rehabilitation, Medical University of Gdansk, Gdansk, Poland
Jaroslaw Slawek*
Affiliation:
Department of Neurology, St. Adalbert Hospital, Gdansk, Poland Department of Psychiatric- Neurological Nursing, Medical University of Gdansk, Gdansk, Poland
*
Jaroslaw Slawek, Department of Neurology, St. Adalbert Hospital, Al. Jana Pawla II 50, 80-462 Gdansk, Poland. Tel: +48 58 768 4661; Fax: +48 58 340 9290; E-mail: jaroslawek@gumed.edu.pl

Extract

Soltan W, Sitek E, Wichowicz H, Wieczorek D, Slawek J. Abnormal gait and bradykinesia in the preclinical phase of Huntington's disease – psychogenic movement disorder?

Objective: Psychiatric symptoms may occur in individuals at risk of Huntington's disease (HD) regardless of their genetic status. Psychopathological symptomatology is attributed to both genetic and environmental factors. In case of asymptomatic gene carriers, psychiatric symptoms may precede involuntary movements.

Methods: We report the first case with abnormal gait and bradykinesia in preclinical adult HD. A 33-year-old woman blind to her mother's HD diagnosis and her own genetic status developed motor slowing and gait disturbance. The symptoms withdrew due to counselling and antidepressant medications. Subsequently, she was informed her own and her mother's genetic testing results, but 2-year follow-up did not reveal the onset of choreic movements, cognitive deterioration or depressive symptoms in the patient. Personality assessment (Minnesota Multiphasic Personality Inventory) and neurological examination results are presented, accompanied by 2-year follow-up data. Follow-up examination included Unified Huntington's Disease Rating Scale (motor, behaviour and function), Beck Depression Inventory, Hamilton Depression Rating Scale and neuropsychological assessment (trail-making test, Stroop test, verbal fluency trials, symbol digit modalities test, digit span, serial seven subtraction, Hopkins verbal learning test and nine-hole peg test).

Conclusion: Motor abnormalities in individuals at risk of HD may be of psychogenic origin. It is a matter of debate if this psychogenic reaction presented as hypokinetic syndrome may be a result of choreic movements of her mother (hyperkinetic syndrome) and depression or if this psychogenic reaction represents the preclinical psychiatric abnormalities in an asymptomatic gene carrier preceding the onset of the disease.

Type
Case Reports
Copyright
Copyright © Cambridge University Press 2011

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1.Rosenblatt, A, Leroi, I.Neuropsychiatry of Huntington's disease and other basal ganglia disorders. Psychosomatics 2000;41:2430.CrossRefGoogle ScholarPubMed
2.Paulsen, JS, Langbehn, DR, Stout, JC et al. Detection of Huntington's disease decades before diagnosis: the Predict-HD study. J Neurol Neurosurg Psychiatry 2008;79:874880.CrossRefGoogle ScholarPubMed
3.Julien, CL, Thompson, JC, Wild, S et al. Psychiatric disorders in preclinical Huntington's disease. J Neurol Neurosurg Psychiatry 2007;78:939943.CrossRefGoogle ScholarPubMed
4.Arrojo-Romero, M, Silva, AF, Palha, AP.Hipocondria and Huntington's disease [Hypochondriasis and Huntington's disease]. Actas Esp Psiquiatr 2006;34:6566.Google ScholarPubMed
5.Williams, DT, Ford, B, Fahn, S.Phenomenology and psychopathology related to psychogenic movement disorders. Adv Neurol 1995;65:233257.Google ScholarPubMed
6.Berrios, GE, Wagle, AC, Markova, IS, Wagle, SA, Rosser, A, Hodges, JR.Psychiatric symptoms in neurologically asymptomatic Huntington's disease gene carriers: a comparison with gene negative at risk subjects. Acta Psychiatr Scand 2002;105:224230.CrossRefGoogle ScholarPubMed
7.Nowak, DA, Fink, GR.Psychogenic movement disorders: aetiology, phenomenology, neuroanatomical correlates and therapeutic approaches. Neuroimage 2009;47:10151025.CrossRefGoogle ScholarPubMed
8.Ginovart, N, Lundin, A, Farde, L et al. PET study of the pre- and post-synaptic dopaminergic markers for the neurodegenerative process in Huntington's disease. Brain 1997;120:503514.CrossRefGoogle ScholarPubMed
9.Kägi, G, Bhatia, KP, Tolosa, E.The role of DAT-SPECT in movement disorders. J Neurol Neurosurg Psychiatry 2010;81:512.CrossRefGoogle ScholarPubMed