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Plasma delta sleep inducing peptide (DSIP) is elevated in symptomatic depressed and remitted depressed patients
Neurobiology of Depression
BIOL PSYCHIATRY 1989;25:148A-152A
149A
able to classify correctly 83.8% of S, 73.9% of NS, and 80% of patients overall. Cognitive impairment was not related to AM or PM levels of ACTH or pre-dex plasma cortisol; but, UFC did correlate significantly with deterioration in cognitive performance. The association between DST status and neuropsychological performance, though, was more robust. We conclude that in some depressed patients, both HPA dysregulation and cognitive impairment appear to be downstream results of a central disturbance. Studies of hippocampal degeneration due to glucocorticoid exposure, and changes associated with aging, provide evidence consistent with this hypothesis.
300 EEG DISTURBANCES ARE RELATED TO NAP SLEEP AND TRYPTOPHAN RESPONSE IN ELDERLY PATIENTS Eliezer Perl, David Gurevich, Curtis Bagne, Das Kareti, Abul-Foiz Hossain-Imam, Manuel Dumlao, Robert Levine, Donald Caldwell Detroit, MI
Serotonergic transmitter deficiency exists in dementia and in depression. Effects of tryptophan (LT), a serotonergic enhancer, on daytime naps and their relation to EEG disturbances were studied. Subjects were demented (N = 16) depressed (N = 23) and normal elders (N = 12), ages 58-85 years. The study procedure included a standard EEG and three sleep lab sessions. Session one was for accommodation to sleep lab. Three grams of LT or placebo (PL) were given randomly, at noon, double blind, before sessions two and three. All sessions began at Ipm, after lunch. Polysomnography recording method and scoring technique followed Rechtschaffen and Kales procedures. EEG reports were scored as normal, mildly abnormal or pathological. Mean sleep latencies on placebo for subjects with normal, mildly abnormal or pathological EEGs were 17.9, 12.4, and 8.3 minutes (df = 2138, F = 3.09, p < .06). Mean differences in percent of stage one sleep between LT and PL sessions were 2.6, -9.8, and -21.5 (df = 2/40, F = 3.21, p < .05) and those in percent of stage two sleep were -3.9, 7.9, and 26.2 correspondingly (df = 2140, F = 3.92, p < .03). EEG pathology was related to diagnosis but the relations between EEG and sleep variables were markedly different from those between diagnosis and sleep variables. Pathological EEG tends to be related, beyond diagnosis, to increased somnolence and to increased intensity of sleep following LT load and both phenomena are of potential clinical and physiological interest.
301 PLASMA DELTA SLEEP INDUCING PEPTIDE (DSIP) IS ELEVATED IN SYMPTOMATIC DEPRESSED AND REMITTED DEPRESSED PATIENTS Ingbert E. Fuchs, John W. Cain, John R. Debus, Howard P. Roffwarg, Robin B. Jarrett, Monica A. Basco, Brad Witte, A. John Rush Dallas, TX The nonpeptide DSIP has been isolated from cerebral venous blood of rabbits subjected
to thalamic stimulation DSIP-like immunoreactivity (LIR) is found in rabbits, dogs, human plasma, and human CSF. One study reveals lower and another reports higher
15OA
BIOL PSYCHIATRY 1989;25:148A-152A
Neurobiology of Depression
plasma DSIP-LIR in depressed patients. Twelve normal controls, 12 symptomatic depressed, and ten remitted depressed patients were studied after 14 drug-free days. Patients were diagnosed by DSM-III-R and RDC. Normals were free of personal and familial psychopathology. 0800 samples were measured for DSIP-LIR by RIA. DSIPLIR levels (pg/ml plasma) were 693.9 (SD = 73.9) in normals, 872.9 (SD = 87.4) in depressed, and 790.4 (SD = 63.6) in remitted depressed subjects. DSIP-LIR levels were lower in normals than in the symptomatic (p < .OOl) and remitted (p < .OOl) groups. Seven of 12 (58%) symptomatic depressed and three of ten (30%) remitted depressed subjects fell outside the normal range. Sleep EEG measures were obtained on both the symptomatic and remitted depressed patients. Correlational analyses between DSIP-LIR levels and selected sleep EEG parameters will be presented.
AND BIOLOGICAL VULNERABILITY 302 PSYCHOLOGICAL DEPRESSION IN HIGH-RISK RELATIVES Donna E. Giles, David J. Kupfer, Howard P. Roffwarg Pittsburgh,
TO
PA
In an ongoing study of risk factors for depression in first-degree relatives of unipolar depressed probands, we have assessed EEG sleep and cognitive variables (beliefs, attributional style, moment-to-moment thinking) in relatives of (1) reduced REM latency (0 minutes) depressed probands, (2) nonreduced REM latency ( > 65.0 minutes) depressed probands, and (3) normal control probands. To date, there are ( 1) 25 asymptomatic relatives of reduced REM latency probands, (2) 42 asymptomatic relatives of nonreduced REM latency probands, and (3) 23 relatives of normal control probands. Cognitive variables did not discriminate between relatives of normal control probands and non-reduced REM latency probands. Reduced REM latency occurred more frequently in the families of reduced REM latency probands (p < .03); these relatives also had a higher lifetime prevalence of depression (p < .03). None were symptomatic at assessment, yet these relatives had higher scores on tests of beliefs, attributional style, and moment-to-moment thinking, as is found during an episode. These relatives may be at risk, both biologically and psychologically, for depression.
303 WEIGHT CHANGE AND SLEEP CONTINUITY IN MAJOR DEPRESSIVE DISORDER Timothy Hsu, James E. Shipley, John F. Greden, Alan S. Eiser, Alan B . Douglass, Roger F. Haskett, Leon J. Grunhaus, Atul C. Pande Ann Arbor, MI
A retrospective analysis was done to compare the effects of weight change alone on sleep measures in depressed patients. All patients had a primary RDC diagnosis of MDD. Subjects were divided into two groups according to whether they reported a loss or gain of 2-20 kg weight over the course of their depressive episode. Subjects who reported no significant weight change, change of more than 2 20 kg, or who had a major medical problem were excluded. The two groups combined included 60 subjects with 43 losers and 17 gainers. After two weeks drug-free, all patients had two nights of EEG sleep recorded. A number of significant differences were noted in sleep
BIOL PSYCHIATRY 1989;25:148A-152A
149A
able to classify correctly 83.8% of S, 73.9% of NS, and 80% of patients overall. Cognitive impairment was not related to AM or PM levels of ACTH or pre-dex plasma cortisol; but, UFC did correlate significantly with deterioration in cognitive performance. The association between DST status and neuropsychological performance, though, was more robust. We conclude that in some depressed patients, both HPA dysregulation and cognitive impairment appear to be downstream results of a central disturbance. Studies of hippocampal degeneration due to glucocorticoid exposure, and changes associated with aging, provide evidence consistent with this hypothesis.
300 EEG DISTURBANCES ARE RELATED TO NAP SLEEP AND TRYPTOPHAN RESPONSE IN ELDERLY PATIENTS Eliezer Perl, David Gurevich, Curtis Bagne, Das Kareti, Abul-Foiz Hossain-Imam, Manuel Dumlao, Robert Levine, Donald Caldwell Detroit, MI
Serotonergic transmitter deficiency exists in dementia and in depression. Effects of tryptophan (LT), a serotonergic enhancer, on daytime naps and their relation to EEG disturbances were studied. Subjects were demented (N = 16) depressed (N = 23) and normal elders (N = 12), ages 58-85 years. The study procedure included a standard EEG and three sleep lab sessions. Session one was for accommodation to sleep lab. Three grams of LT or placebo (PL) were given randomly, at noon, double blind, before sessions two and three. All sessions began at Ipm, after lunch. Polysomnography recording method and scoring technique followed Rechtschaffen and Kales procedures. EEG reports were scored as normal, mildly abnormal or pathological. Mean sleep latencies on placebo for subjects with normal, mildly abnormal or pathological EEGs were 17.9, 12.4, and 8.3 minutes (df = 2138, F = 3.09, p < .06). Mean differences in percent of stage one sleep between LT and PL sessions were 2.6, -9.8, and -21.5 (df = 2/40, F = 3.21, p < .05) and those in percent of stage two sleep were -3.9, 7.9, and 26.2 correspondingly (df = 2140, F = 3.92, p < .03). EEG pathology was related to diagnosis but the relations between EEG and sleep variables were markedly different from those between diagnosis and sleep variables. Pathological EEG tends to be related, beyond diagnosis, to increased somnolence and to increased intensity of sleep following LT load and both phenomena are of potential clinical and physiological interest.
301 PLASMA DELTA SLEEP INDUCING PEPTIDE (DSIP) IS ELEVATED IN SYMPTOMATIC DEPRESSED AND REMITTED DEPRESSED PATIENTS Ingbert E. Fuchs, John W. Cain, John R. Debus, Howard P. Roffwarg, Robin B. Jarrett, Monica A. Basco, Brad Witte, A. John Rush Dallas, TX The nonpeptide DSIP has been isolated from cerebral venous blood of rabbits subjected
to thalamic stimulation DSIP-like immunoreactivity (LIR) is found in rabbits, dogs, human plasma, and human CSF. One study reveals lower and another reports higher
15OA
BIOL PSYCHIATRY 1989;25:148A-152A
Neurobiology of Depression
plasma DSIP-LIR in depressed patients. Twelve normal controls, 12 symptomatic depressed, and ten remitted depressed patients were studied after 14 drug-free days. Patients were diagnosed by DSM-III-R and RDC. Normals were free of personal and familial psychopathology. 0800 samples were measured for DSIP-LIR by RIA. DSIPLIR levels (pg/ml plasma) were 693.9 (SD = 73.9) in normals, 872.9 (SD = 87.4) in depressed, and 790.4 (SD = 63.6) in remitted depressed subjects. DSIP-LIR levels were lower in normals than in the symptomatic (p < .OOl) and remitted (p < .OOl) groups. Seven of 12 (58%) symptomatic depressed and three of ten (30%) remitted depressed subjects fell outside the normal range. Sleep EEG measures were obtained on both the symptomatic and remitted depressed patients. Correlational analyses between DSIP-LIR levels and selected sleep EEG parameters will be presented.
AND BIOLOGICAL VULNERABILITY 302 PSYCHOLOGICAL DEPRESSION IN HIGH-RISK RELATIVES Donna E. Giles, David J. Kupfer, Howard P. Roffwarg Pittsburgh,
TO
PA
In an ongoing study of risk factors for depression in first-degree relatives of unipolar depressed probands, we have assessed EEG sleep and cognitive variables (beliefs, attributional style, moment-to-moment thinking) in relatives of (1) reduced REM latency (0 minutes) depressed probands, (2) nonreduced REM latency ( > 65.0 minutes) depressed probands, and (3) normal control probands. To date, there are ( 1) 25 asymptomatic relatives of reduced REM latency probands, (2) 42 asymptomatic relatives of nonreduced REM latency probands, and (3) 23 relatives of normal control probands. Cognitive variables did not discriminate between relatives of normal control probands and non-reduced REM latency probands. Reduced REM latency occurred more frequently in the families of reduced REM latency probands (p < .03); these relatives also had a higher lifetime prevalence of depression (p < .03). None were symptomatic at assessment, yet these relatives had higher scores on tests of beliefs, attributional style, and moment-to-moment thinking, as is found during an episode. These relatives may be at risk, both biologically and psychologically, for depression.
303 WEIGHT CHANGE AND SLEEP CONTINUITY IN MAJOR DEPRESSIVE DISORDER Timothy Hsu, James E. Shipley, John F. Greden, Alan S. Eiser, Alan B . Douglass, Roger F. Haskett, Leon J. Grunhaus, Atul C. Pande Ann Arbor, MI
A retrospective analysis was done to compare the effects of weight change alone on sleep measures in depressed patients. All patients had a primary RDC diagnosis of MDD. Subjects were divided into two groups according to whether they reported a loss or gain of 2-20 kg weight over the course of their depressive episode. Subjects who reported no significant weight change, change of more than 2 20 kg, or who had a major medical problem were excluded. The two groups combined included 60 subjects with 43 losers and 17 gainers. After two weeks drug-free, all patients had two nights of EEG sleep recorded. A number of significant differences were noted in sleep