P3 and contingent negative variation in Parkinson's disease

Friedemann Pulvermüller, Werner Lutzenberger, Viktor Müller, Bettina Mohr, Johannes Dichgans, Niels Birbaumer

Research output: Contribution to journalArticle

Abstract

Patients with idiopathic Parkinson's syndrome, most of them in early stages of the disease, and matched healthy controls participated in a continuous performance task while their EEGs were recorded from 15 electrodes. During preparation of movements, a contingent negative variation (CNV) maximal at central and posterior sites was visible. This CNV was reduced in the patient population. A large P3-like 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 inhibition between such cortico-striatal cell assemblies is mediated by the neostriatum, the forebrain structure primarily affected in Parkinson's disease.

Original languageEnglish
Pages (from-to)456-467
Number of pages12
JournalElectroencephalography and Clinical Neurophysiology
Volume98
Issue number6
DOIs
Publication statusPublished - Jun 1996

Keywords

  • Cell assembly
  • Contingent negative variation
  • Continuous performance task
  • Cortex
  • P3
  • Parkinson
  • Striatum

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

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  • Cite this

    Pulvermüller, F., Lutzenberger, W., Müller, V., Mohr, B., Dichgans, J., & Birbaumer, N. (1996). P3 and contingent negative variation in Parkinson's disease. Electroencephalography and Clinical Neurophysiology, 98(6), 456-467. https://doi.org/10.1016/0013-4694(96)95537-6