Does increased gamma activity in patients suffering from Parkinson’s disease counteract the movement inhibiting beta activity?

Akinesia and rigidity are cardinal symptoms of Parkinson's disease (PD). Previous studies analysing event-related desynchronization during movement onset associated both symptoms with pathologically increased oscillations in the beta frequency range. By focusing on the movement onset only, these studies cannot, however, shed light onto the question how oscillatory activity is changed during continuous movements. To investigate this issue, we compared the power of the local field potentials (LFP) within and above the subthalamic nucleus (STN) during rest, an isometric hold condition of the forearm, and a fist flexion and extension task in 13 patients with idiopathic PD during implantation of deep brain stimulation (DBS) electrodes. During fist flexion and extension (relative to rest), significantly increased activity in the low beta (12-18 Hz) and gamma (30-48 Hz) frequency ranges was observed within the STN, while during hold (compared to rest) no significant difference was found. For the regions above the STN the power during fist movements (compared to rest) was significantly higher, i.e. in the range of 18-30 Hz, with no significant changes in the gamma frequency range. Beta activity is claimed to inhibit movement and thereby could render fist movements more exhausting. Therefore, the observed increase in beta activity in the STN during fist movements might result in bradykinesia as experienced by many patients. We hypothesise that in order to enable repetitive fist movement despite increased beta activity, "prokinetic" gamma activity may be increased as a compensatory mechanism.