title: Relationship between oscillations in the basal ganglia and synchronization of cortical activity.
abstract: The functions of oscillations within the basal ganglia are poorly understood. We discuss in the present paper, the possible physiological or pathological roles of oscillatory activities within the basal ganglia, and their relationship to cortical oscillations. Three aspects are presented: 1. What do we know from animal studies? 2. What do we know from neurophysiological studies in parkinsonian patients? 3. What is the effect of L-dopa treatment and electrical stimulation within basal ganglia circuits on cortical oscillations? Animal studies suggest that neuronal oscillations are spontaneously generated within the basal ganglia system, especially from the GPE and the subthalamic nucleus (STN), but are mainly synchronized by cortical activity via the striatal inputs. Dopamine depletion results in a global increase of oscillations within the whole basal ganglia system, particularly in the GP-NST network. Oscillations within the basal ganglia may, in part, be related to tremor since they are enhanced, especially in the globus pallidus internus (GPI) and the STN, in human and animal dopaminergic depletion. However, they also play a role in the physiology of movement as revealed by coherence analysis between cortex, muscles and GPI/STN in parkinsonian patients undergoing deep brain stimulation. It is known that the basal ganglia may influence cortico-muscular oscillations such as the Piper rhythm and other rhythms in the beta band. In off-drug parkinsonian patients, low frequency oscillations (4-10 Hz) are favoured, presumably resulting in bradykinesia and low force. When medically (Ldopa) or surgically (deep brain stimulation) treated, these low frequency oscillations are replaced by high frequency (70 Hz) oscillations that are important for motor programs to be correctly executed. Studies of cortical reactivity related to planning of voluntary movement in parkinsonian patients provide evidence that it is possible to influence cortical reactivity through the basal ganglia system.
authors.affiliation: Service de Neurophysiologie clinique, Hôpital Roger-Salengro, CHRU de Lille, 59037 Lille Cedex, France.
authors.forename: François
authors.initials: F
authors.lastname: Cassim
authors.forename: Etienne
authors.initials: E
authors.lastname: Labyt
authors.forename: David
authors.initials: D
authors.lastname: Devos
authors.forename: Luc
authors.initials: L
authors.lastname: Defebvre
authors.forename: Alain
authors.initials: A
authors.lastname: Destée
authors.forename: Philippe
authors.initials: P
authors.lastname: Derambure
mesh_terms: D000818:Animals; D001479:Basal Ganglia / Q000502:physiology* / Q000503:physiopathology; D002540:Cerebral Cortex / Q000502:physiology* / Q000503:physiopathology; D004298:Dopamine / Q000502:physiology; D006801:Humans; D009068:Movement / Q000502:physiology; D014202:Tremor / Q000503:physiopathology
chemical_list: D004298:Dopamine