Electrophysiology of the prefrontal cortex in healthy controls and schizophrenic patients: a review

Authors
Citation
Aj. Fallgatter, Electrophysiology of the prefrontal cortex in healthy controls and schizophrenic patients: a review, J NEURAL TR, 108(6), 2001, pp. 679-694
Citations number
88
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEURAL TRANSMISSION
ISSN journal
03009564 → ACNP
Volume
108
Issue
6
Year of publication
2001
Pages
679 - 694
Database
ISI
SICI code
0300-9564(2001)108:6<679:EOTPCI>2.0.ZU;2-4
Abstract
Prefrontal brain regions, in particular the anterior cingular gyrus (ACG), are altered in chronic schizophrenic patients and also play a pivotal role in physiological mechanisms of response control. A cued Continuous Performa nce Test (CPT) is a suitable paradigm for the investigation of response con trol, as it contains its fundamental mechanisms, i.e. the execution (Go) an d the inhibition (NoGo) of an anticipated motor response. Previous electrop hysiological investigations in healthy subjects during CPT execution reveal ed that the gravity center (centroid) of the event-related potential (ERP) elicited during the NoGo-condition is located more anterior as compared to the Go-condition in every single case. Moreover, by means of an electrophys iological source location method this NoGo-anteriorisation phenomenon (NGA) has been attributed to a strong brain electrical NoGo-hyperactivity locate d in prefrontal brain areas (ACG). Furthermore, the NGA has a superior test -retest reliability, a very high interindividual stability and is independe nt from age- and gender-effects. Systematic schizophrenic patients were cha racterized by a significantly diminished NGA indicating a dysfunction of pr efrontal brain areas including the ACG. Based on these findings, the NGA ha s to be considered as a first electrophysiological measure for the quantita tive assessment of ACG-function within a response control paradigm. Hopeful ly, this biological parameter will contribute to the elucidation of the eti opathogenetical background in different schizophrenic diseases.