title: Surface electromyography shows increased mirroring in Parkinson's disease patients without overt mirror movements.
abstract: Patients with Parkinson's disease (PD) may present mirror movements (MM). Transcranial magnetic stimulation data indicate that these movements reflect an abnormal enhancement of the "physiological mirroring" that can be observed in healthy adults during complex and effortful tasks. It was hypothesized that, in PD, enhanced mirroring is caused by a failure of basal ganglia output to support the cortical network that is responsible for the execution of strictly unimanual movements. If so, it is likely that subtle alterations of voluntary unimanual motor control are also present in PD patients without overt MM. We tested this hypothesis by using surface electromyographic (EMG) techniques in 12 mildly to moderately affected PD patients without overt MM, and in 2 control groups (12 age-matched and 10 young healthy volunteers). Subjects performed unilateral phasic thumb abduction during a sustained tonic contraction of the opposite abductor pollicis brevis. All patients were tested on dopaminergic therapy. On a separate day, 7 of 12 patients were re-tested after withdrawal of medication. During this task, involuntary mirror-like increase in surface EMG of the tonically abducting thumb was significantly larger in PD patients than in age-matched or young healthy volunteers. Off therapy, mirroring was slightly greater than on medication, although this difference was not significant. Our findings suggest that dysfunction of unimanual motor control is a general feature of PD. It is likely that this deficient movement lateralization contributes to an impairment of nonsymmetrical bimanual movements in PD.
authors.affiliation: Unit of Neurology, Santa Maria Nuova Hospital, Florence, Italy. cincotta@unifi.it
authors.forename: Massimo
authors.initials: M
authors.lastname: Cincotta
authors.forename: Fabio
authors.initials: F
authors.lastname: Giovannelli
authors.forename: Alessandra
authors.initials: A
authors.lastname: Borgheresi
authors.forename: Fabrizio
authors.initials: F
authors.lastname: Balestrieri
authors.forename: Paola
authors.initials: P
authors.lastname: Vanni
authors.forename: Aldo
authors.initials: A
authors.lastname: Ragazzoni
authors.forename: Gaetano
authors.initials: G
authors.lastname: Zaccara
authors.forename: Ulf
authors.initials: U
authors.lastname: Ziemann
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000978:Antiparkinson Agents / Q000627:therapeutic use; D001479:Basal Ganglia / Q000187:drug effects / Q000503:physiopathology; D002540:Cerebral Cortex / Q000187:drug effects / Q000503:physiopathology; D018491:Dopamine Agonists / Q000627:therapeutic use; D004576:Electromyography / Q000187:drug effects; D005260:Female; D007839:Functional Laterality / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D007537:Isometric Contraction / Q000187:drug effects / Q000502:physiology; D007980:Levodopa / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D009415:Nerve Net / Q000187:drug effects / Q000503:physiopathology; D010300:Parkinson Disease / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology*; D011712:Pyramidal Tracts / Q000187:drug effects / Q000503:physiopathology; D012016:Reference Values
chemical_list: D000978:Antiparkinson Agents; D018491:Dopamine Agonists; D007980:Levodopa