Parkinson’s Disease (PD) is a neurodegenerative disorder primarily impacting motor control. Research into the neurophysiological basis of PD often uses tremor or gait impairment as the motor end-point due to their ease of assessment. However, rigidity is another important symptom to encapsulate the motor presentation of the disease state, which is rarely tracked digitally and typically assessed only by a clinician passively moving the patient’s limbs. Additionally, a common limitation of PD research is the inability to modulate symptomatic severity in a controlled manner, instead relying on dramatic contrasts between an individual’s medicated and unmedicated states. In this project we present a novel motor control paradigm seeking to address these deficits.

Using a robotic wrist manipulandum participants were subject to a destabilisation phase of short, forceful perturbations from the robot while attempting to stabilise the robot’s handle at a centralised position. Participants were then presented with a visual cue to perform voluntary flexion (F) or extension (E) movement of the wrist to a target. Participants were next passively moved through the range of FE movement by the robot to quantify rigidity as a measure of resistance to smooth, external, low-amplitude force. During the protocol, participants’ neural activity was recorded through EEG while motor and behavioural data was collected using EMG sensors and integrated force and positional data from the robot.

Testing has focussed on the application of this paradigm to healthy controls (HCs) with the intent to assess which features defining the destabilisation phase were most significant in modulating the participant’s rigidity. Frequency, amplitude and temporal uniformity of perturbations were investigated.

Investigation of 14 HCs subject to both high (10) and low (5) perturbation schedules has shown that increased perturbation count results in slower voluntary movement following the destabilisation phase (p=0.012, paired t-test) while reaction time is not significantly differentiated (p=0.080, paired t-test).

Preliminary investigation of the impact of perturbation amplitude contrasting 1Nm and 0.5Nm perturbations on 5 HCs has suggested that higher amplitude of perturbation results in slower voluntary movement but no change in reaction time. Computing co-contraction indices (CCIs) of the antagonist muscle pairing during the robot-led passive movement as a computation of rigidity has so far proven inconclusive.

The preliminary findings confirm the potential to effectively modulate wrist rigidity in HCs using only mechanical perturbations. Future work includes exploration of the neural data as well as application of the finalised paradigm to PD patients is required.