Search

Parkinson’s disease (PD) is characterized by decreased dopamine in the basal ganglia that causes excessive tonic inhibition of the thalamus. This excessive inhibition seems to explain inhibitory motor symptoms in PD, but the source of tremor remains unclear. This paper investigates how neural inhibition may change the closed-loop characteristics of the human motor control system to determine how this established pathophysiology could produce tremor. The rate-coding model of neural signals suggests increased inhibition decreases signal amplitude, which could create a mismatch between the closed-loop dynamics and the internal models that overcome proprioceptive feedback delays. This paper aims to identify a candidate model structure with decreased-amplitude-induced tremor in PD that also agrees with previously recorded movements of healthy and cerebellar patients. The optimal feedback control theory of human motor control forms the basis of the model. Key additional elements include gating of undesired movements via the basal ganglia-thalamus-motor cortex circuit and the treatment of the efferent copy of the control input as a measurement in the state estimator. Simulations confirm the model’s ability to capture tremor in PD and also demonstrate how disease progression could affect tremor and other motor symptoms, providing insight into the existence of tremor and non-tremor phenotypes. Altogether, the physiological underpinnings of the model structure and the agreement of model predictions with clinical observations provides support for the hypothesis that unstable feedback produces parkinsonian tremor. Consequently, these results also support the associated framework for the neuroanatomy of human motor control. [ABSTRACT FROM AUTHOR]

Active wearable tremor suppression devices apply actuators to the human body to produce joint torques that reduce tremor motion. This potential alternative to medications and surgery has the advantage of providing robust tremor treatment that is non-invasive, but the bulkiness of typical engineering actuators currently prohibits clinical implementations. Dielectric elastomer stack actuators (DESAs) offer a potential pathway towards achieving soft, low-profile tremor suppression devices: DESAs have similar mechanical properties as human muscles and can conform to the human limb. However, low actuation levels and a lack of commercial availability limit the development of DESA-based orthoses. Employing a control approach that only suppresses tremor while allowing the actuators to follow voluntary motion passively significantly decreases actuation requirements to improve potential for clinical devices. Still, DESAs that may offer the necessary actuation characteristics require specialized equipment and techniques. This research advances DESA-based tremor suppression by experimentally demonstrating DESA-based suppression of tremor-like signals on a scaled system using easily manufactured DESAs. Further discussion quantifies the DESA parameters that will enable physical implementations of human-scale tremor suppression and identifies pathways towards achieving those parameters. [ABSTRACT FROM AUTHOR]