Oknina,L., Juran, S., Oades, R. D., Weisbrod,M. (a), Chan, E., Chen, E. Y. H. (b), Röpcke, B., (2004).
Frontal and temporal lobe sources for mismatch negativity (MMN) in schizophrenia: an ERP and MR-anatomical imaging study.
Schizophrenia Research, 67 (supplement), p. 22.

Biopsychology Group, University Clinic for Child and Adolescent Psychiatry, Essen, Germany: Oades@uni-essen.de. (a) University Psychiatry Clinic, Heidelberg, Germany, (b) Queen Mary Hospital, University of Hong Kong, PRC

.Introduction: MMN is an electrophysiological measure of automatic auditory change detection. A smaller MMN in patients with schizophrenia (Ref. 1, 2) may reflect altered frontal activity (Ref. 3).

Methods: We studied
Following our report on the coordinates for frontal and temporal lobe dipole-loci contributing to normal MMN (Ref. 4) we replicated this result using brain electrical source analysis (BESA) and MR-images of the brain in 14 healthy subjects (34.8y) and compared it with 17 patients (32 y) 15 years after the onset of schizophrenia. .

Results:
First:
a) For MMN associated with a frequency deviant tone asymmetric loci in the superior-temporal and left anterior-cingulate gyri were replicated, while that in the right inferior-frontal gyrus moved to the mid-frontal border (residual variance [RV] <1%). turnover:
Second:
Patients showed a modest MMN reduction, a weaker left temporal lobe source but essentially similar loci (RV~1%).
Third:
a) Discrete changes in the locus of left temporal and cingulate sources were illustrated by plotting volumes around the group solution for individual’s data to 2% RV, with the radius illustrating the standard deviation of the distance to the better solutions for other subjects’ loci (also using a 2% RV criterion).
b) The left temporal lobe source was marginally more medial in patients (5 mm, p<0.01), while the left cingulate was more rostral (10 mm, p<0.0001).

Conclusions: The data show a degree of compensation of function despite altered source locations in the left hemisphere.

1. Oades et al. 1995 EEG Clin Neurophysiol 44, 428-438. (Oades et al., 1995).
2. Umbricht et al 2002 Biol Psychiat 53, 1120-1131
3. Baldeweg et al 2002 Int J Psychophysiol 43, 111-122
4. Jemel et al 2002 Brain Topog 15, 13-27. (Jemel et al., 2002).
Dr. Oknina was supported by the Alfried Krupp von Bohlen und Halbach Stiftung