Maintaining balance against force perturbations: impaired mechanisms unresponsive to levodopa in Parkinson's disease.
There is evidence that postural instability associated with Parkinson's disease (PD) is not adequately improved by levodopa, implying involvement of nondopaminergic pathways. However, the mechanisms contributing to postural instability have yet to be fully identified and tested for their levodopa responsiveness. In this report we investigate balance processes that resist external forces to the body when standing. These include in-place responses and the transition to protective stepping. Forward and backward shoulder pulls were delivered using two force-feedback-controlled motors and were randomized for direction, magnitude, and onset. Sixteen patients with PD were tested OFF and ON levodopa, and 16 healthy controls were tested twice. Response behavior was quantified from 3-dimensional ground reaction forces and kinematic measurements of body segments and total body center-of-mass (CoM) motion. In-place responses resisting the pull were significantly smaller in PD as reflected in reduced horizontal anteroposterior ground reaction force and increased CoM displacement. Ankle, knee, and hip moments contributing to this resistance were smaller in PD, with the knee extensor moment to backward pulls being the most affected. The threshold force needed to evoke a step was also smaller for PD in the forward direction. Protective steps evoked by suprathreshold pulls showed deficits in PD in the backward direction, with steps being shorter and more steps being required to arrest the body. Levodopa administration had no significant effect on either in-place or protective stepping deficits. We conclude that processes employed to maintain balance in the face of external forces show impairment in PD consistent with disruption to nondopaminergic systems.
Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, London, United Kingdom;
Irene
I
Di Giulio
Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, London, United Kingdom; School of Medicine, University of Tasmania, Hobart, Australia; and.
Rebecca J
RJ
St George
Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, London, United Kingdom; St. Luke's Hospital, Thessaloniki, Greece.
Eirini
E
Kalliolia
Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, London, United Kingdom;
Amy L
AL
Peters
Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, London, United Kingdom;
Patricia
P
Limousin
Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, London, United Kingdom; brian.day@ucl.ac.uk.
Brian L
BL
Day
D000368:Aged; D000978:Antiparkinson Agents / Q000627:therapeutic use; D001696:Biomechanical Phenomena; D025461:Feedback, Physiological / Q000187:drug effects; D005260:Female; D005684:Gait / Q000187:drug effects / Q000502:physiology; D006801:Humans; D007596:Joints / Q000294:innervation; D007980:Levodopa / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D009068:Movement / Q000187:drug effects; D010300:Parkinson Disease / Q000150:complications* / Q000188:drug therapy*; D004856:Postural Balance / Q000187:drug effects / Q000502:physiology*; D012678:Sensation Disorders / Q000188:drug therapy / Q000209:etiology*
D000978:Antiparkinson Agents; D007980:Levodopa
Parkinson's disease; balance; dopaminergic pathways; levodopa; postural instability; pull test