Universität zu Köln

Hasan, Alkomiet, Wobrock, Thomas, Grefkes, Christian ORCID: 0000-0002-1656-720X, Labusga, Marcin, Levold, Katrin, Schneider-Axmann, Thomas, Falkai, Peter ORCID: 0000-0003-2873-8667, Mueller, Hendrik, Klosterkoetter, Joachim and Bechdolf, Andreas (2012). Deficient Inhibitory Cortical Networks in Antipsychotic-Naive Subjects at Risk of Developing First-Episode Psychosis and First-Episode Schizophrenia Patients: A Cross-Sectional Study. Biol. Psychiatry, 72 (9). S. 744 - 752. NEW YORK: ELSEVIER SCIENCE INC. ISSN 1873-2402

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Abstract

Background: Impaired cortical inhibition is a well-established finding in schizophrenia patients and has been linked to dysfunctional gamma-aminobutyric acid (GABA)ergic transmission. However, there have been no previous studies investigating cortical excitability with particular regard to intracortical inhibitory networks in antipsychotic-naive subjects at risk of developing first-episode psychosis. Methods: A total of 18 subjects at risk, 18 first-episode schizophrenia patients, and 18 healthy control subjects were included in this study. Transcranial magnetic stimulation over the left primary motor cortex was used to determine short-latency intracortical inhibition, intracortical facilitation, and the contralateral silent period (CSP). Short-latency intracortical inhibition can be considered as a parameter of GABA type A (GABA(A))-mediated inhibition and it has been proposed that CSP can test GABA type B (GABA(B))-mediated inhibitory intracortical networks. Results: Subjects at risk and first-episode patients showed a reduced short-latency intracortical inhibition compared with healthy control subjects, suggesting reduced GABA(A)-mediated inhibition. First-episode patients had a prolonged CSP duration compared with the other two groups, implying a GABA(B) imbalance only in patients with full-blown psychosis. Analyses did not reveal group differences for intracortical facilitation. Conclusions: These results indicate specific alterations in inhibitory cortical networks in subjects at risk and in first-episode patients. It appears that there is already a cortical inhibitory deficit in at-risk individuals. These results suggest a possible GABA(A) dysfunction early in the disease course, whereas alterations in GABA(B) functionality seem to occur later in the disease's progression. Future longitudinal studies will be needed to clarify this inhibitory deficit and its relation to the transition to psychosis.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Hasan, Alkomiet UNSPECIFIED UNSPECIFIED UNSPECIFIED Wobrock, Thomas UNSPECIFIED UNSPECIFIED UNSPECIFIED Grefkes, Christian UNSPECIFIED orcid.org/0000-0002-1656-720X UNSPECIFIED Labusga, Marcin UNSPECIFIED UNSPECIFIED UNSPECIFIED Levold, Katrin UNSPECIFIED UNSPECIFIED UNSPECIFIED Schneider-Axmann, Thomas UNSPECIFIED UNSPECIFIED UNSPECIFIED Falkai, Peter UNSPECIFIED orcid.org/0000-0003-2873-8667 UNSPECIFIED Mueller, Hendrik UNSPECIFIED UNSPECIFIED UNSPECIFIED Klosterkoetter, Joachim UNSPECIFIED UNSPECIFIED UNSPECIFIED Bechdolf, Andreas UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-480355
DOI:	10.1016/j.biopsych.2012.03.005
Journal or Publication Title:	Biol. Psychiatry
Volume:	72
Number:	9
Page Range:	S. 744 - 752
Date:	2012
Publisher:	ELSEVIER SCIENCE INC
Place of Publication:	NEW YORK
ISSN:	1873-2402
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language TRANSCRANIAL MAGNETIC STIMULATION; LONG-TERM POTENTIATION; MOTOR CORTEX; NEUROANATOMICAL ABNORMALITIES; SILENT PERIOD; AUDITORY P300; EXPRESSION; PLASTICITY; ONSET; EXCITABILITY Multiple languages Neurosciences; Psychiatry Multiple languages
URI:	http://kups.ub.uni-koeln.de/id/eprint/48035