Slow Brain Potential and Oscillatory EEG Manifestations of Impaired Temporal Preparation in Parkinson's Disease

Performance in behavioral tasks is influenced by temporal expectations shaped by the temporal structure of the task. Such implicit temporal preparation is reflected in slow brain potentials and electroencephalographic oscillations and is attributed to interval timing mechanisms that probably depend on intact basal ganglia function. We investigated implicit timing in Parkinson's disease using a choice reaction task with two temporally regular stimulus presentation regimes, both including occasional deviant interstimulus intervals. Control subjects, but not patients, demonstrated temporal preparation in the form of an adjustment in time course of slow brain potentials to the duration of the interstimulus interval. However, in both groups, timing perturbations were accompanied by a slow brain potential amplitude drop at the time of expected stimulus occurrence, demonstrating intact representation of time in patients. In patients, oscillatory activity in beta and alpha bands showed attenuated preparatory desynchronization and reduced postmovement event-related synchronization, reflecting abnormal engagement and disengagement of sensorimotor and parietal areas. The results demonstrate profoundly deficient temporal preparation with preserved encoding of temporal information, a dissociation that may be explained by impaired dopamine-dependent motor learning. The results are discussed in the context of recent work on oscillatory activity in the basal ganglia.

Malfunctions of Central Control of Movement Studied with Slow Brain Potentials in Neurological Patients

Studies are reviewed that used movement-related EEG potentials to investigate impairments of movement control in neurological patients. The EEG potentials reviewed are the Bereitschaftspotential (BP), Contingent Negative Variation (CNV), and components of the lateralized readiness potential (LRP). Patient groups included in this review are patients with infarction of the middle cerebral artery, Parkinson's disease, cerebellar disease, and amyotrophic lateral sclerosis. A rich body of evidence has been collected on Parkinson's disease, and somewhat less on cerebellar atrophy, contributing to an understanding of the impairments caused by these diseases. In contrast, not much research has been done in amyotrophic lateral sclerosis and in infarction patients. The latter is particularly striking since utility of this method for assessing residual capacities of affected motor areas seems rather obvious.