Introduction: Anesthetics such as propofol likely exert their influence by altering functional connectivity within different brain circuits. However, network level analyses of anesthesia, particularly in humans have been sparse due to limited access to concurrent intracranial and subcortical recordings. Here, we aim to gain insight into the effects of propofol on pallidocortical circuits in Parkinson disease (PD) patients, with specific attention to alpha (8-13 Hz) and beta (13-35 Hz) oscillations, implicated in the “akinetic” state of the basal-ganglia thalamocortical (BGTC) motor network.
Methods: We recorded local field potentials from sensorimotor cortices and pallidum, in twelve PD patients undergoing DBS implantation surgery targeting globus pallidus internus (GPi), while subjects were resting with their eyes open and after propofol-induced loss of consciousness (LOC). We measured spectral power and connectivity (de-biased weighted phase lag index) between pallidum and sensory-motor cortices during rest and after LOC.
Results: At all nodes, propofol anesthesia shifts the dominant spectral peak toward alpha frequencies while increasing low frequency (<20 Hz) power. In GPi, power in frequencies >20 Hz decreases. At the cortical level however, there is broadband power increase (20-100 Hz) across all cortices with power suppression in frequencies > 200 Hz specific to the premotor cortex. Propofol also causes a shift in the pallidocortical connectivity such that alpha-low beta (8-20 Hz) connectivity increases whereas high beta (20-35 Hz) connectivity decreases.
Conclusions: Alpha oscillations are suggested to functionally inhibit unneeded neuronal networks during movement. Our findings suggest that propofol-induced increase in alpha synchronization may be the underpinning for propofol-induced immobility, in addition to suppression of beta synchrony (both local and inter-regional). Moreover, recent discoveries in PD pathophysiology suggest that it is most likely excessive coupling between nodes of the BGTC motor network that are related to disease symptoms. Reduction of pallidocortical high beta coupling with propofol further supports this hypothesis.
Patient Care: This study is informative for the recording method and aiming to understand anesthetic-induced alterations in motor network connectivity, providing an improved understanding that could be use to both monitor Parkinson disease and help decipher mechanisms of anesthesia. The knowledge gained contributes toward understanding disease pathoophysiology and will inform the design of closed-loop systems, all of which can lead to improving the quality of life of PD patients.
Learning Objectives: 1) Understanding the effects of propofol on sensorimotor cortical electrophysiology
2) Understanding the effects of propofol on subcortical (pallidal) electrophysiology
3) Understanding changes in pallidocortical synchrony as they relate to propofol and Pakrinson disease