Clozapine increases EEG photic driving in clinical responders.

Photically driven electroencephalography was tested in 17 chronic schizophrenia patients who were treated with clozapine for 5 weeks. Eight of the 17 patients showed clinical improvement on the Brief Psychiatric Rating Scale (delta BPRS > 30%) while the other 9 patients remained unchanged (delta BPRS < 15%). In comparison with the nonresponders, clozapine responders had a significantly greater increase in photic driving in the electroencephalogram (EEG), primarily in the low-frequency range of alpha band (7.2 hertz [Hz], 8.3 Hz, 9.0 Hz, and 9.6 Hz, but not 12.0 Hz). The difference in the resting EEG between the responders and nonresponders did not reach statistical significance. These findings suggested that EEG photic driving might be more sensitive than the resting EEG in detecting the central nervous system drug effect. Further analysis revealed that the increase of EEG photic driving was positively correlated with patients' clinical improvement. Combined with our previous observation in the drug-free schizophrenia patients who had lower EEG photic driving, present results supported the hypothesis that the amount of EEG alpha activity, particularly its synchronization to the external stimuli, could reflect the thalamic function in sensory information processing in schizophrenia.

[1]  B. Saletu,et al.  Drug profiling by computed electroencephalography and brain maps, with special consideration of sertraline and its psychometric effects. , 1988, The Journal of clinical psychiatry.

[2]  Hemispheric Lateralization of Fast EEG Activity in Schizophrenia and Endogenous Depression , 1981 .

[3]  D. Regan.  Human brain electrophysiology: Evoked potentials and evoked magnetic fields in science and medicine , 1989 .

[4]  CHAPTER FOUR – Role of the Thalamus in Sleep Control: Sleep–Wakefulness Studies in Chronic Diencephalic and Athalamic Cats1 , 1974 .

[5]  S. Potkin,et al.  EEG alpha photic driving abnormalities in chronic schizophrenia , 1989, Psychiatry Research.

[6]  R. Morison,et al.  ELECTRICAL ACTIVITY OF THE THALAMUS AND BASAL GANGLIA IN DECORTICATE CATS , 1945 .

[7]  F. D. Silva.  Neural mechanisms underlying brain waves: from neural membranes to networks. , 1991 .

[8]  R. Llinás,et al.  The functional states of the thalamus and the associated neuronal interplay. , 1988, Physiological reviews.

[9]  J. Panksepp.  Advances in Biological Psychiatry , 1996 .

[10]  J. Overall,et al.  The Brief Psychiatric Rating Scale , 1962 .

[11]  W. Clark,et al.  Principles of psychopharmacology , 1978 .

[12]  A. Oke,et al.  Elevated thalamic dopamine: possible link to sensory dysfunctions in schizophrenia. , 1987, Schizophrenia bulletin.

[13]  E. Adrian.  Afferent discharges to the cerebral cortex from peripheral sense organs , 1941, The Journal of physiology.

[14]  J. Small,et al.  Computerized EEG profiles of haloperidol, chlorpromazine, clozapine and placebo in treatment resistant schizophrenia. , 1987, Clinical EEG.

[15]  J. Roubicek,et al.  Computer analysed EEG and behavioral changes after psychoactive drugs. , 1975, International journal of neurology.

[16]  M. Geyer,et al.  Startle habituation and sensorimotor gating in schizophrenia and related animal models. , 1987, Schizophrenia bulletin.

[17]  R Isenhart,et al.  Abnormal EEG responses to photic stimulation in schizophrenic patients. , 1990, Schizophrenia bulletin.

[18]  J. Schlag,et al.  Basic sleep mechanisms , 1974 .