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Abnormal gait and bradykinesia in the preclinical phase of Huntington's disease – psychogenic movement disorder?
Published online by Cambridge University Press: 24 June 2014
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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.
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