ELSEVIER Electroencephalographyand clinical Neurophysiology 98 (1996) 456--467 P3 and contingent negative variation in Parkinson's disease Friedemann Pulvermtiller a, Werner Lutzenberger a, Viktor Mtillera, Bettina Mohr% Johannes Dichgans b, Niels Birbaumer ~,c alnstitut fiir Medizinische Psychologic und Verhaltensneurobiologie, Universitdt Tiibingen, 72074 Tiibingen, Germany bNeurologische Klinik, Universitiit Tiibingen, 72074 Tiibingen, Germany CUniversita degli Studi, Padova, Italy Accepted for publication: 25 January 1996 Abstract Patients with idiopathic Parkinson's syndrome, most of them in early stages of the disease, and matched healthy controls partici- pated in a continuous performance task while their EEGs were recorded from 15 electrodes. During preparation of movements, a con- tingent negative variation (CNV) maximal at central and posterior sites was visible. This CNV was reduced in the patient population. A large P3-1ike positive deflection occurred after go and no-go stimuli that called for execution (go) or suppression (no-go) of a button press. Compared to healthy controls, the positive wave in Parkinson patients was significantly reduced after go stimuli and maximally attenuated when no-go stimuli had indicated to suppress the motor response. In contrast, P3 amplitudes after irrelevant 'ignore' stimuli was not significantly reduced in the patients. These results are interpreted in the framework of a model of striatal function postulating (i) that populations of cortical and striatal neurons form distributed functional units (Hebbian cell assemblies), and (ii) that mutual in- hibition between such cortico-striatal cell assemblies is mediated by the neostriatum, the forebrain structure primarily affected in Park- inson's disease. Keywords: Cell assembly; Contingent negative variation; Continuous performance task; Cortex; P3; Parkinson; Striatum 1. Introduction Recent years have seen the development of increas- ingly precise theories specifying the role of the basal ganglia in the complex interplay of brain nuclei and corti- ces. This study aims at testing predictions of a theory about basal ganglia function using non-invasive record- ings of electrocortical responses from patients with Park- inson's disease. Using evoked potentials and slow poten- tial shifts to investigate electrophysiological correlates of a disease primarily affecting structures deep inside the brain may appear insufficient at first glance. The primary source of evoked potentials is neuronal activity in the upper layers of cortex. It is primarily the simultaneous occurrence of numerous excitatory post synaptic poten- tials at apical dendrites of pyramidal neurons close to the recording electrode that causes changes in the evoked * Corresponding author. Tel.: +49 7071 294220; fax: +49 7071 295956; e-mail: pumue@uni-tuebingen.de. potential at the surface of the head (Birbaumer et al., 1990). Why, therefore, should a disturbance primarily affecting basal ganglia function, such as Parkinson's dis- ease, lead to changes of evoked responses? The answer to this question is evident from what is known about the connections between basal ganglia and cortex. While a large number of cortical areas project to the neostriatum (the phylogenetically 'new' part of the striatum), the neostriatum itself projects back to various areas of the frontal lobes of the cortex. The pathway from neostriatum to cortex passes through the pallidum (or paleostriatum, the phylogenetically old part of the striatum) and through motor nuclei of the thalamus (VL and VA) (Cote and Crutcher, 1991). The thalamo-cortical connections in- volved in this loop terminate in the upper cortical layers, where they contact apical dendrites of pyramidal neurons. This implies that activity at the termination of the cortico- striato-thalamo-cortical loop can be monitored in surface recordings. A disease affecting basal ganglia function may, therefore, lead to an electrophysiological change visible in evoked electrocortical responses. 0013-4694/96/$12.00 © 1996 Elsevier Science Ireland Ltd. All rights reserved PII S0921-884X(96)95537-3 EEG 95537