title: Rhythmic movement in Parkinson's disease: effects of visual feedback and medication state.
abstract: Previous studies examining discrete movements of Parkinson's disease (PD) patients have found that in addition to performing movements that were slower than those of control participants, they exhibit specific deficits in movement coordination and in sensorimotor integration required to accurately guide movements. With medication, movement speed was normalized, but the coordinative aspects of movement were not. This led to the hypothesis that dopaminergic medication more readily compensates for intensive aspects of movement (such as speed), than for coordinative aspects (such as coordination of different limb segments) (Schettino et al., Exp Brain Res 168:186-202, 2006). We tested this hypothesis on rhythmic, continuous movements of the forearm. In our task, target peak speed and amplitude, availability of visual feedback, and medication state (on/off) were varied. We found, consistent with the discrete-movement results, that peak speed (intensive aspect) was normalized by medication, while accuracy, which required coordination of speed and amplitude modulation (coordinative aspect), was not normalized by dopaminergic treatment. However, our findings that amplitude, an intensive aspect of movement, was also not normalized by medication, suggests that a simple pathway gain increase does not act to remediate all intensive aspects of movement to the same extent. While it normalized movement peak speed, it did not normalize movement amplitude. Furthermore, we found that when visual feedback was not available, all participants (PD and controls) made faster movements. The effects of dopaminergic medication and availability of visual feedback on movement speed were additive. The finding that movement speed uniformly increased both in the PD and the control groups suggests that visual feedback may be necessary for calibration of peak speed, otherwise underestimated by the motor control system.
authors.affiliation: Biological Engineering Department, Massachusetts Institute of Technology, Cambridge, MA, USA.
authors.forename: S
authors.initials: S
authors.lastname: Levy-Tzedek
authors.forename: H I
authors.initials: HI
authors.lastname: Krebs
authors.forename: J E
authors.initials: JE
authors.lastname: Arle
authors.forename: J L
authors.initials: JL
authors.lastname: Shils
authors.forename: H
authors.initials: H
authors.lastname: Poizner
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000978:Antiparkinson Agents / Q000494:pharmacology* / Q000627:therapeutic use; D056228:Feedback, Sensory / Q000187:drug effects / Q000502:physiology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009068:Movement / Q000187:drug effects / Q000502:physiology*; D010300:Parkinson Disease / Q000188:drug therapy / Q000503:physiopathology*; D010507:Periodicity; D010775:Photic Stimulation / Q000379:methods*; D011597:Psychomotor Performance / Q000187:drug effects / Q000502:physiology*; D013028:Space Perception / Q000187:drug effects / Q000502:physiology
chemical_list: D000978:Antiparkinson Agents