The Non-Motor Symptoms Scale is an acceptable, reproducible, valid, and precise assessment instrument for nonmotor symptoms in Parkinson disease.

Background: Postural instability in Parkinson's disease (PD) can lead to falls, injuries and reduced quality of life. We investigated whether balance in PD can improve by offering patients feedback about their own trunk sway as a supplement to natural sensory inputs. Specifically, we investigated the effect of artificial vibrotactile biofeedback on trunk sway in PD. Methods: Twenty PD patients were assigned to a control group (n ¼ 10) or biofeedback group (n ¼ 10). First, all patients performed two sets of six gait tasks and six stance tasks (pre-training assessment). Subsequently, all subjects trained six selected tasks five times (balance training). During this training, the feedback group received vibrotactile feedback of trunk sway, via vibrations delivered at the head. After training, both groups repeated all twelve tasks (post-training assessment). During all tasks, trunk pitch and roll movements were measured with angular velocity sensors attached to the lower trunk. Outcomes included sway angle and sway angular velocity in the roll and pitch plane, and task duration. Results: Overall, patients in the feedback group had a significantly greater reduction in roll (P ¼ 0.005) and pitch (P < 0.001) sway angular velocity. Moreover, roll sway angle increased more in controls after training, suggesting better training effects in the feedback group (P < 0.001). Conclusions: One session of balance training in PD using a biofeedback system showed beneficial effects on trunk stability. Additional research should examine if these effects increase further after more intensive training, how long these persist after training has stopped, and if the observed effects carry over to non-trained tasks.

Motor imagery (MI) is widely used to study cognitive aspects of the neural control of action. Prior studies were mostly centred on hand and arm movements. Recently a few studies have used imagery tasks to explore the neurophysiology of human gait, but it remains unclear how to ascertain whether subjects actually perform imagery of gait as requested. Here we describe a new experimental protocol to quantify imagery of gait, by behaviourally distinguishing it from visual imagery (VI) processes and by showing its temporal correspondence with actual gait. Fourteen young healthy subjects performed two imagery tasks and an actual walking (AW) task. During both imagery tasks subjects were sitting on a chair and faced a computer screen that presented photographs of walking trajectories. During one task (MI), subjects had to imagine walking along the walking trajectory. During the other task (VI), subjects had to imagine seeing a disc moving along the walking trajectory. During the AW task, subjects had to physically walk along the same walking trajectory as presented on the photographs during the imagery tasks. We manipulated movement distance by changing the length of the walking trajectory, and movement difficulty by changing the width of the walking trajectory. Subjects reported onset and offset of both actual and imagined movements with a button press. The time between the two button presses was taken as the imagined or actual movement time (MT). MT increased with increasing path length and decreasing path width in all three tasks. Crucially, the effect of path width on MT was significantly stronger during MI and AW than during VI. The results demonstrate a high temporal correspondence between imagined and AW, suggesting that MI taps into similar cerebral resources as those used during actual gait. These results open the possibility of using this protocol for exploring neurophysiological correlates of gait control in humans.

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In Parkinson's disease (PD) subtle balance abnormalities can already be detected in early-stage patients. One feature of impaired balance control in PD is asymmetry: one leg produces more corrective joint torque than the other. We hypothesize that in mild to moderately affected PD patients, the least impaired leg compensates for the more impaired leg. Twenty PD patients and eleven healthy matched control subjects participated. Clinical asymmetry was determined by the difference between the left and right body side scores on the Unified Parkinson's Disease Rating Scale. Balance was perturbed with two independent continuous multisine perturbations in the forward-backward direction. Subsequently, we applied closed-loop system identification, which determined the spectral estimate of the stabilizing mechanisms, for each leg. Balance control behavior was similar in PD patients and control subjects at the ankle, but at the hip stiffness was increased. Control subjects exhibited symmetric balance control, but in PD patients the balance contribution of the leg of the clinically least affected body side was higher whereas the leg of the clinically most affected body side contributed less. The ratio between the legs helped to preserve a normal motor output at the ankle. Our results suggest that PD patients compensate for balance control asymmetries by increasing the relative contribution of the leg of their least affected body side. This compensation appears to be successful at the ankle but is accompanied by an increased stiffness at the hip. We discuss the possible implications of these findings for postural stability and fall risk in PD patients.