Journal of the International Neuropsychological Society


Syntactic language processing: ERP lesion data on the role of the basal ganglia

SONJA A.  KOTZ  a1 a2 c1 , STEFAN  FRISCH  a1 a3 , D. YVES  VON CRAMON  a1 a2 and ANGELA D.  FRIEDERICI  a1
a1 Max-Planck-Institute of Cognitive Neuroscience, Leipzig, Germany
a2 Day Care Clinic of Cognitive Neurology, University of Leipzig, Germany
a3 Institute of Linguistics, University of Potsdam, Germany

Article author query
kotz sa   [PubMed][Google Scholar] 
frisch s   [PubMed][Google Scholar] 
von cramon dy   [PubMed][Google Scholar] 
friederici ad   [PubMed][Google Scholar] 


The role of the basal ganglia in syntactic language processing was investigated with event-related brain potentials in fourteen neurologically impaired patients. Seven of these patients had basal ganglia lesions while 7 other patients primarily had lesions of the left temporo–parietal region excluding the basal ganglia. All patients listened to sentences that were either correct or included a verb argument structure violation. In previous experiments this type of violation elicited a biphasic pattern of an N400–P600 complex in young healthy participants. While the N400 may result from incorrect semantic-thematic role assignment, the P600 reflects the fact that verb information does not license the syntactic structure at present. Results of the patient experiment revealed a double dissociation: patients with left temporo–parietal lesions only show a P600, whereas patients with lesions of the basal ganglia showed no P600, but a negativity with extended duration that resembled an N400. The latter pattern not only confirms previous reports that the basal ganglia modulate the P600 but extends these results by showing that the N400 as a late semantic–thematic integration process appears partially modulated by the basal ganglia. (JINS, 2003, 9, 1053–1060.)

(Received January 15 2003)
(Revised April 28 2003)
(Accepted May 2 2003)

Key Words: Basal ganglia; Event-related brain potentials (ERPs); E(L)AN; P600; N400.

c1 Reprint requests to: Sonja A. Kotz, Max-Planck-Institute of Cognitive Neuroscience, PO Box 500 355, D-04303 Leipzig, Germany. E-mail: