Neuromagnetic Evidence of Abnormal Movement-Related Beta Desynchronization in Parkinson's Disease

Abstract

Parkinson's disease (PD) is a neurodegenerative disorder associated with debilitating motor, posture, and gait abnormalities. Human studies recording local field potentials within the subthalamic nucleus and scalp-based electroencephalography have shown pathological beta synchronization throughout the cortical–basal ganglia motor network in PD. Suppression of such pathological beta synchronization has been associated with improved motor function, which may explain the effectiveness of deep-brain stimulation. We used magnetoencephalography (MEG) to investigate neural population-level beta responses, and other oscillatory activity, during a motor task in unmedicated patients with PD and a matched group of healthy adults. MEG is a noninvasive neurophysiological technique that permits the recording of oscillatory activity during movement planning, execution, and termination phases. Each of these phases was independently examined using beamforming to distinguish the brain areas and movement phases, where pathological oscillations exist during motor control. Patients with PD exhibited significantly diminished beta desynchronization compared with controls prior to and during movement, which paralleled reduced alpha desynchronization. This study is the first to systematically investigate neural oscillatory responses in PD during distinct stages of motor control (e.g. planning, execution, and termination) and indicates that these patients have significant difficulty suppressing cortical beta synchronization during movement planning, which may contribute to their diminished movement capacities.

Distinct Roles for Alpha- and Beta-Band Oscillations during Mental Simulation of Goal-Directed Actions

“…Previous studies investigating task-induced modulations of alpha-and beta-band power have not identified the dissociation shown in this study (Pfurtscheller and Lopes da Silva, 1999;de Lange et al, 2008;Bauer et al, 2012;ter Horst et al, 2013;Heinrichs-Graham et al, 2014). However, those studies did not investigate differential effects of task demand on spectral profiles nor included a neutral control condition.…”

Deep brain stimulation: a mechanistic and clinical update

“…In addition to excess b, PD patients were found to have diminished g response amplitude and peak frequency. 78 Taken together, these data fit into the model proposed by Shimamoto and colleagues in which excess motor cortical b synchrony, manifesting clinically as hypokinesia, is a result of strong pathological b oscillations passed from the basal ganglia. 177 This increased cortical b synchronization, in turn, leads to reinforcement of the basal ganglia b oscillations through pathological M1 b-phase g-amplitude coupling (Fig.…”

Circadian modulation of motor-related beta oscillatory responses

“…Briefly, there is an event-related desynchronization (ERD) in the beta-frequency range (14–28 Hz) that peaks before movement onset and continues slightly after movement execution, which is termed the pre-movement beta ERD response. There is an event-related synchronization (ERS) in the gamma-frequency range that coincides with the onset of movement and is relatively brief (i.e., ~200 ms), and finally there is a post-movement beta ERS that reaches maximum amplitude slightly after the termination of movement (Cheyne et al, 2008; Gaetz et al, 2010, 2011; Hall et al, 2011; Heinrichs-Graham et al, in press; Jurkiewicz et al, 2006; Tzagarakis et al, 2010; Wilson et al, 2010, 2011). This latter response is generally termed the post-movement beta rebound (PMBR).…”