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Diazepam binding inhibitor and sleep EEG in schizophrenia
Sleep
BIOL PSYCHIATRY 1992;31:61A-252A
167A
244 DIAZEPAM BINDING INHIBITOR AND SLEEP EEG IN
SCHIZOPHRENIA Daniel P. van Kammen, Jeffrey L. Peters, Alessandro Guidotti, Thomas Neylan, Andrew Mouton, Mar,,, E. Kelley, Mark Gilbertson, John Gurklis, Erminio Costa HDVAMC, Pittsburgh, PA 15206. Based on the sleep-inducing and potential antipsychotic effects of benzodiazepines (BZDs), and the relationships between, negative schizophrenic symptoms and rapid eye movement (REM) sleep latency and slow wave sleep, we ~*udied CSF diazepam-binding inhibitor-like immunoreactivity (DBI-ir) and polysomnography in schizophrenic patients. Twenty-eight. drug-free male schizophrenic patients underwent a 3 night polysomnography evaluation and a lumbar puncture. CSF DBl-ir cow-related positively with REM latency and stage 4% sleep, and correlated negatively with stage 1% sleep and REM deasity. The results of this first study of the relationship between endogenous DBI and sleep in humans s~ggest a different physiological role for DBI than concluded from pharmacological studies. However, the absence of similar sleep data in normals precludes us from establishing a specific relationship between DBI and sleep in schizophrenia.
245 AGE EFFECTS ON EEG SLEEP IN ALCOHOLICS James E. Shipley, Michael S. Aldrich, Rajiv Tandon, Phillip D. Kroll, Kirk J. Brower University of Michigan, Ann A.rbor, Mi 48109.0840. Sleep complaints are prominent in alcoholics, but the pathephysiology of these changes is not well understood. To further characterize EEG sleep patterns in alcoholics, we studied 38 alcoholics by DIS and 20 controls for 2 consecutive nights after a 2-week drug-free period. Data for the second night were used for analysis. Patients were in treatment, and overt depression was rare. Mean age was 38.9 years (range 2357) in the patients and 38.6 years (range 23-64) in controls. Alcoholics had consistently impaired sleep continuity and lighter sleep. REM latency was significantly shorter in the patients (46.8 - 35.2 versus 66.4 _ 25.4 re!a, p < 0.05) and REM % was increased (25.1 ± 6.5 versus 21.1 ± 4.1, p < 0.05), but REM activity and REM density did not differ between the groups. Age and REM latency were negatively correlated in both controls (r -- -0.47, ,~ < 0.05) and patients (r - -0.39, p < 0.0% Controls tended to have stronger correlations between age and various measures of sleep depth and quality. This may be due to "premature aging" in alcoholics, resulting in consistently poor sleep in patients regardless of age. Patients showed positive correlations between age and REM % (r -- 0.34, p < 0.0S), REM activity (r -0.40, p < 0.05), and REM density (r - 0.31, p < 0.06), whereas controls did ~:ot. We conclude that age is a significant factor contributing to sleep abnormalities in alcoholics. The fin61ngs of shortened REM latency, increased REM percent, and a disease-specific association of age wi~h hm'eased REM pressure suggest potential overlap with the pathophysiology of major depression. Further research will include a direct comparison to patients with MDD, and will assess the possible association of subtle depressive symptoms with these REM sleep findings in alcoholics.
BIOL PSYCHIATRY 1992;31:61A-252A
167A
244 DIAZEPAM BINDING INHIBITOR AND SLEEP EEG IN
SCHIZOPHRENIA Daniel P. van Kammen, Jeffrey L. Peters, Alessandro Guidotti, Thomas Neylan, Andrew Mouton, Mar,,, E. Kelley, Mark Gilbertson, John Gurklis, Erminio Costa HDVAMC, Pittsburgh, PA 15206. Based on the sleep-inducing and potential antipsychotic effects of benzodiazepines (BZDs), and the relationships between, negative schizophrenic symptoms and rapid eye movement (REM) sleep latency and slow wave sleep, we ~*udied CSF diazepam-binding inhibitor-like immunoreactivity (DBI-ir) and polysomnography in schizophrenic patients. Twenty-eight. drug-free male schizophrenic patients underwent a 3 night polysomnography evaluation and a lumbar puncture. CSF DBl-ir cow-related positively with REM latency and stage 4% sleep, and correlated negatively with stage 1% sleep and REM deasity. The results of this first study of the relationship between endogenous DBI and sleep in humans s~ggest a different physiological role for DBI than concluded from pharmacological studies. However, the absence of similar sleep data in normals precludes us from establishing a specific relationship between DBI and sleep in schizophrenia.
245 AGE EFFECTS ON EEG SLEEP IN ALCOHOLICS James E. Shipley, Michael S. Aldrich, Rajiv Tandon, Phillip D. Kroll, Kirk J. Brower University of Michigan, Ann A.rbor, Mi 48109.0840. Sleep complaints are prominent in alcoholics, but the pathephysiology of these changes is not well understood. To further characterize EEG sleep patterns in alcoholics, we studied 38 alcoholics by DIS and 20 controls for 2 consecutive nights after a 2-week drug-free period. Data for the second night were used for analysis. Patients were in treatment, and overt depression was rare. Mean age was 38.9 years (range 2357) in the patients and 38.6 years (range 23-64) in controls. Alcoholics had consistently impaired sleep continuity and lighter sleep. REM latency was significantly shorter in the patients (46.8 - 35.2 versus 66.4 _ 25.4 re!a, p < 0.05) and REM % was increased (25.1 ± 6.5 versus 21.1 ± 4.1, p < 0.05), but REM activity and REM density did not differ between the groups. Age and REM latency were negatively correlated in both controls (r -- -0.47, ,~ < 0.05) and patients (r - -0.39, p < 0.0% Controls tended to have stronger correlations between age and various measures of sleep depth and quality. This may be due to "premature aging" in alcoholics, resulting in consistently poor sleep in patients regardless of age. Patients showed positive correlations between age and REM % (r -- 0.34, p < 0.0S), REM activity (r -0.40, p < 0.05), and REM density (r - 0.31, p < 0.06), whereas controls did ~:ot. We conclude that age is a significant factor contributing to sleep abnormalities in alcoholics. The fin61ngs of shortened REM latency, increased REM percent, and a disease-specific association of age wi~h hm'eased REM pressure suggest potential overlap with the pathophysiology of major depression. Further research will include a direct comparison to patients with MDD, and will assess the possible association of subtle depressive symptoms with these REM sleep findings in alcoholics.