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Clozapine concentrations and changes in alpha EEG power
180A
BIOL PSYCHIATRY 1991;29:43A- 185A
Eleetrophysiology and Neurophysiology
300 CLOZAPINE CONCENTRATIONS AND CHANGES IN
ALPHA EEG POWER Yi Jin, M.D., Angela McCraw, B.A., Kathy Mann, R.N., Lynette Asselin, Steven G. Potkin, M.D. Universio' of California Irvine Medical Center, Orange, CA 92668. Spectra of 24-hr photic driving EEG following a single dose of 50 mg ciozapine (po) in eight drug-free schizoplarenic patients were studied to clarify the relationship between plasma clozapine concentrations and brain effects. Modeled pharmacokinetic examinations showed that the drug plasma concentration paralleled the change of EEG photic driving power with a specific lag t i m . The hysteresis curve had the same shape in all subjects although the lag time was not constant between subjects. A single dose of clozapine clearly increased alpha EEG power following phoric &~,,ing reflected by a nonlinear relationship to plasma clozapine con,.-entrations. The reasons that ~he EEG did not linearly refl~t clozapine blood levels may be due to differences in physiologica.~ processes: (1) drug perftmion, (2) diffusion, (3) partitioning, and (4) receptor events. The variation in pharmacokinetic parameters should be considered in pharmaco-EEG studies.
301 EXPLORING THE "SENSORY GATING" PHENOMENON
Yossi Guterman, Ph.D., Richard C. Josiassen, Ph.D. The Medical College of Pennsylvania/EPPL Philadelphia, PA 19129. In order to investigate possible attentional aspects of the auditory P.s0 sensory gating (SG) phenomenon (Adler et al 1982), ten healthy subjects were exposed to the conditioning-testing paradigm and to three modified conditions that varied in processing and response demands regarding the second stimulus (count/no count: simple motor reactions; go/no go). In addition, four comparable blocks of single stimulus trials provided a baseline to assess the effect of the warning stimulus. An average 61% suppression of P.sooccurred with passive exposure, which represents a replication of the original finding. However, this suppression disappeared in the count/no count condition and was intermediate in the two motor-reactL'm-related conditions. P.so responses in all single stimulus blocks were larger than in the paired conditions, and unaffected by processing/response demands. The results sugges: that SG may be a special case of an attention regulation process tt~at is triggered by the warning stimulus, with the activating or inhibitory nature determined by the processing and response demands of the task. The warning stim'_'!'_,emay have aa additional, indiscriminately suppressing effect, operating independently of this attention regulation process.
302 ABNORMAL EEG SLEEP IN CHILDREN: A HYPOTHESIS
Donna E. Giles, Howard P. Roffwarg, David J. Kupfer Universit3' of Pittsburgh School of Medicine, Pittsburgh, PA 15213, and Universi~." :?f Texas Southwestern Medical Center at Dallas. EEG sleep abnormalities aggregate in adult relatives of unipolar probands with reduced REM latency (Giles et al 1989). These abnormalities do not simply reflect a history of depression, since abnormalitie~ occurred in unafl(ected relatives. Abnormal EEG sleep has not been reliably observed in depressed children. The disparity between findings in depressed children and adults may be secondary to maturational influences on EEG sleep, based on evidence for age-dependent EEG sleep changes in normal children and no differences between depressed children and controls. Yet EEG sleep abnormalities have been observed in depressed children. We hypothesized that EEG sleep abnormalities occur in children with both a family history of depression and abnormal parental EEG sleep. Thirteen parents and 15 offspring were studies in the sleep laboratory. All subjects had a family history of major depression. Eight of 13 parents had reduced REM latency. Correlations between parent and offspring EEG sleep were greater than 0.35 for REM latency (0.36-0.39), REM density (0.58--0.64), REM time (0.39-0.50), stage 2 sleep (0.51-0.62), slow-wave
BIOL PSYCHIATRY 1991;29:43A- 185A
Eleetrophysiology and Neurophysiology
300 CLOZAPINE CONCENTRATIONS AND CHANGES IN
ALPHA EEG POWER Yi Jin, M.D., Angela McCraw, B.A., Kathy Mann, R.N., Lynette Asselin, Steven G. Potkin, M.D. Universio' of California Irvine Medical Center, Orange, CA 92668. Spectra of 24-hr photic driving EEG following a single dose of 50 mg ciozapine (po) in eight drug-free schizoplarenic patients were studied to clarify the relationship between plasma clozapine concentrations and brain effects. Modeled pharmacokinetic examinations showed that the drug plasma concentration paralleled the change of EEG photic driving power with a specific lag t i m . The hysteresis curve had the same shape in all subjects although the lag time was not constant between subjects. A single dose of clozapine clearly increased alpha EEG power following phoric &~,,ing reflected by a nonlinear relationship to plasma clozapine con,.-entrations. The reasons that ~he EEG did not linearly refl~t clozapine blood levels may be due to differences in physiologica.~ processes: (1) drug perftmion, (2) diffusion, (3) partitioning, and (4) receptor events. The variation in pharmacokinetic parameters should be considered in pharmaco-EEG studies.
301 EXPLORING THE "SENSORY GATING" PHENOMENON
Yossi Guterman, Ph.D., Richard C. Josiassen, Ph.D. The Medical College of Pennsylvania/EPPL Philadelphia, PA 19129. In order to investigate possible attentional aspects of the auditory P.s0 sensory gating (SG) phenomenon (Adler et al 1982), ten healthy subjects were exposed to the conditioning-testing paradigm and to three modified conditions that varied in processing and response demands regarding the second stimulus (count/no count: simple motor reactions; go/no go). In addition, four comparable blocks of single stimulus trials provided a baseline to assess the effect of the warning stimulus. An average 61% suppression of P.sooccurred with passive exposure, which represents a replication of the original finding. However, this suppression disappeared in the count/no count condition and was intermediate in the two motor-reactL'm-related conditions. P.so responses in all single stimulus blocks were larger than in the paired conditions, and unaffected by processing/response demands. The results sugges: that SG may be a special case of an attention regulation process tt~at is triggered by the warning stimulus, with the activating or inhibitory nature determined by the processing and response demands of the task. The warning stim'_'!'_,emay have aa additional, indiscriminately suppressing effect, operating independently of this attention regulation process.
302 ABNORMAL EEG SLEEP IN CHILDREN: A HYPOTHESIS
Donna E. Giles, Howard P. Roffwarg, David J. Kupfer Universit3' of Pittsburgh School of Medicine, Pittsburgh, PA 15213, and Universi~." :?f Texas Southwestern Medical Center at Dallas. EEG sleep abnormalities aggregate in adult relatives of unipolar probands with reduced REM latency (Giles et al 1989). These abnormalities do not simply reflect a history of depression, since abnormalitie~ occurred in unafl(ected relatives. Abnormal EEG sleep has not been reliably observed in depressed children. The disparity between findings in depressed children and adults may be secondary to maturational influences on EEG sleep, based on evidence for age-dependent EEG sleep changes in normal children and no differences between depressed children and controls. Yet EEG sleep abnormalities have been observed in depressed children. We hypothesized that EEG sleep abnormalities occur in children with both a family history of depression and abnormal parental EEG sleep. Thirteen parents and 15 offspring were studies in the sleep laboratory. All subjects had a family history of major depression. Eight of 13 parents had reduced REM latency. Correlations between parent and offspring EEG sleep were greater than 0.35 for REM latency (0.36-0.39), REM density (0.58--0.64), REM time (0.39-0.50), stage 2 sleep (0.51-0.62), slow-wave