Polysomnographic and spectral sleep EEG in primary alcoholics: an interaction between alcohol dependence and African-American ethnicity.

BACKGROUND: Disturbances of sleep EEG are prominent in alcoholic patients, persist into recovery, and recently have been found to predict those alcoholics who are most likely to relapse. Increasing evidence indicates that there are ethnic differences in sleep EEG and that African-Americans may be at elevated risk for disordered sleep. METHODS: This study compared polysomnographic and spectral sleep EEG measures in male primary alcoholic inpatients (n = 31) and age-matched comparison controls (n = 31) stratified by African-American and Euro-American ethnicity. RESULTS: African-American alcoholic patients showed more severe sleep abnormalities than Euro-American alcoholics, and the interaction between alcohol dependence and ethnicity uniquely contributed to prolonged sleep latency (p < 0.001), loss of delta sleep (p < 0.001), and short rapid eye movement (REM) latency (p < 0.001). Spectral EEG analyses confirmed polysomnographic findings of disordered sleep architecture in alcoholics. Compared with controls, alcoholics had lower delta (0.75-4.5 Hz) activity over the whole night (p < 0.05), reductions in mean spectral power (0.75-40 Hz, p < 0.05), and decreases of delta (p < 0.01) and theta (4.5-7.5 Hz,p = 0.05) activity during the first period of non-REM sleep, with African-American alcoholics having the lowest theta of the four groups. CONCLUSIONS: In view of the possible connection between relapse and poor sleep and the role of sleep in the maintenance of health, these data have implications for treatment and morbidity outcomes in African-American alcoholics.

Polysomnography and depressive symptoms in primary alcoholics with and without a lifetime diagnosis of secondary depression and in patients with primary major depression.

BACKGROUND: There is evidence suggesting that there is: (1) additive polysomnographic effects of alcoholism and depression; and (2) elevated baseline REM density in primary alcoholics with (PASD) and without lifetime history of secondary depression (NPA). METHODS: 23 PASDs, 59 NPAs, and 23 primary major depression patients (PMD) underwent polysomnography. Any drinking within 3 months after a 1-month inpatient alcohol rehabilitation defined relapse. RESULTS: PASDs' polysomnography was more like NPAs than PMDs. Polysomnography reflected 3-month sobriety status more than diagnosis. LIMITATIONS: Not all PASD's met full major depression criteria upon admission. CONCLUSIONS: Alcoholism affected polysomnography more than depression. Elevated admission REM density predicted 3-month relapse in PASDs and NPAs.

The sleep of abstinent pure primary alcoholic patients: natural course and relationship to relapse.

Sleep in male pure primary alcoholic inpatients was examined at a mean of 16 days (n = 29), 19 weeks (n = 29), 14 months (n = 9), and 27 months (n = 4) of abstinence. Results were as follows: (1) the sleep of abstinent alcoholic patients is short, fragmented, and shallow early in abstinence; (2) a patient's sleep improves slowly over at least the first year of abstinence; however, (3) some facets of a patient's sleep remain abnormal even after 27 months of abstinence; (4) insomnia and sleep fragmentation after approximately 5 months of abstinence may be related to relapse by 14 months. The mechanism underlying the relationship between sleep and withdrawal in alcoholic patients is not well understood, and the issue of treating sleep problems as an adjunct to prevention of relapse warrants further investigation.

Increased REM sleep density at admission predicts relapse by three months in primary alcoholics with a lifetime diagnosis of secondary depression.

BACKGROUND: Having previously reported that 3-month relapse was associated with increased admission REM pressure in nondepressed primary alcoholics, we hypothesized that baseline polysomnography would predict outcome in primary alcoholics with a lifetime diagnosis of secondary depression. METHODS: Twenty-one primary alcoholics with secondary depression received polysomnography and the Hamilton Depression Rating Scale during the first and fourth weeks of a 1-month inpatient alcohol treatment program. Exclusion criteria included serious illness, current major alcohol withdrawal symptoms, other Axis I diagnoses, sleep apnea, nocturnal myoclonus, and psychoactive substances within 14 days of polysomnography. Relapse was defined as drinking any alcohol between hospital discharge and 3-month follow-up. RESULTS: Relapsers' total sleep time was reduced, and REM density (reflecting REM sleep ocular activity) was increased significantly throughout admission compared with abstainers. Sleep continuity and Hamilton scores improved by discharge in sober and relapsing alcoholics. Factors derived from admission REM latency, REM percent, and REM density predicted sobriety vs. relapse within 3 months after hospital discharge in 76% of patients. Admission REM density was greater, and total sleep time was less in relapsers than in patients sober at 3 months. CONCLUSIONS: Results suggest that increased REM density and decreased total sleep time at about 2-4 weeks of abstinence predict relapse by 3 months in depressed alcoholics.

Rapid tryptophan depletion, sleep electroencephalogram, and mood in men with remitted depression on serotonin reuptake inhibitors.

BACKGROUND: In previous studies, depletion of brain serotonin by administration of a tryptophan-free amino acid drink (TFD) (1) temporarily reversed the antidepressant effects of selective serotonin reuptake inhibitors (SSRIs) in euthymic patients who had a history of major depression, and (2) enhanced rapid eye movement (REM) sleep in normal volunteers. In this study, we hypothesized that the TFD would not only increase depressive symptoms but also the propensity for REM sleep in euthymic patients treated with SSRIs. METHODS: Ten fully remitted, medicated male patients who had a history of major depressive episode ingested a 100-g TFD (the experimental dose) or a 25-g TFD (designed to be the control drink) in double-blind, random order on separate days. The effects were assessed with mood ratings, plasma tryptophan concentrations, and an all-night sleep electroencephalogram. RESULTS: The TFDs produced a dose-dependent reduction in plasma tryptophan concentrations, sleep latency, and REM latency, as well as increased REM percentage, REM minutes, REM density, and total sleep time. Neither strength of TFD altered mood to a clinically significant degree. CONCLUSIONS: Although the TFD affected plasma tryptophan concentrations and various sleep measures, our study did not confirm previous reports that TFD temporarily reversed the antidepressant effects of SSRIs in euthymic patients. Our patients, however, had been treated for a longer period with SSRIs and were more fully remitted at the time of the study. Our results suggest that TFD-induced relapse in SSRI-treated patients in remission decreases as a function of treatment duration, degree of remission, or both.

Increased pressure for rapid eye movement sleep at time of hospital admission predicts relapse in nondepressed patients with primary alcoholism at 3-month follow-up.

OBJECTIVE: To determine whether polygraphic sleep recordings, obtained at the time of admission to an inpatient alcohol treatment program, predict abstinence and relapse 3 months following hospital discharge in nondepressed patients with primary alcoholism. DESIGN: Two independent, consecutive cohorts of patients (group 1, n = 28; group 2, n = 17) underwent all-night polygraphic sleep recordings and other clinical evaluations during the first and fourth weeks of a 1-month inpatient treatment program within a Veteran Affairs Medical Center. They were reevaluated 3 months following discharge to the community. None were treated with disulfiram or other medications during or after hospitalization. PATIENTS: All subjects were male veterans with primary alcoholism and without significant preexisting, secondary, or comorbid diagnoses such as major medical problems, depression, antisocial personality, or drug addiction. OUTCOME MEASURES: Relapse was defined as any alcohol consumption between discharge from the hospital and 3-month follow-up. RESULTS: Ten (36%) of 28 patients in group 1 were Relapsers at 3-month follow-up. Relapsers in group 1 showed significantly shorter Rapid Eye Movement (REM) latency, increased Rapid Eye Movement percent (REM%), and increased REM Density during their admission sleep studies compared with Abstainers. To replicate these observations, group 2 was then studied as a validation sample. Six (35%) of 17 patients relapsed. As in group 1, Relapsers had significantly shorter REM latency and increased REM% compared with Abstainers; REM Density was not significantly different in the Relapsers as compared with Abstainers in group 2. Using a principal components analysis based on these three REM sleep measures to determine "REM pressure," three separate discriminant function analyses (DFAs) were calculated: one for each group and one for all patients (n = 45) together. The DFA from group 1 correctly classified 22 (78.6%) of the 28 patients in group 1 and 13 (76.5%) of the 17 patients in group 2 as Relapsers or Abstainers. The DFA from group 2 correctly classified 13 (76.5%) of the 17 patients in group 2 and 23 (82.1%) of the 28 patients in group 1. The DFA formed from both groups together correctly classified 36 (80%) of the 45 patients. When the REM sleep measures at hospital admission and discharge were compared, no statistically significant effect of time was observed. Abstinence and relapse were not consistently related to other clinical measures at the time of hospital admission such as age, duration and severity of alcoholism, marital status, employment, hepatic enzyme levels, cognitive performance, or depression ratings. CONCLUSION: Short REM latency, increased REM%, and, possibly, increased REM Density at the time of admission to a 1-month inpatient alcohol treatment program predict relapse in nondepressed patients with primary alcoholism by 3 months following hospital discharge.