Eating disorders and cocaine abuse: a survey of 259 cocaine abusers.

A structured clinical interview designed to diagnose eating disorders was administered to 259 consecutive callers to the National Cocaine Hotline who met DSM-III criteria for cocaine abuse. Thirty-two percent of those surveyed met DSM-III criteria for either anorexia nervosa, bulimia, or both disorders. The prevalence rates for each of these disorders in this sample appeared elevated even when narrow diagnostic criteria were applied. The data suggest that drug abusers should be screened carefully for the presence of an eating disorder and that abnormalities of eating behaviors seen among these individuals should not be attributed simply to drug use.

Evaluating depression in alcoholics.

The persistence of untreated depression was evaluated in 49 severely depressed alcoholics. After 2 weeks of sobriety, 80% of patients with initial major depression by Research Diagnostic Criteria were no longer depressed. These patients improved without antidepressant medications, suggesting the need for a 2-week period of sobriety before psychopharmacotherapy for depression is instituted. Many severe depressions in actively drinking or recently sober alcoholics may represent alcohol-induced organic affective syndromes which, unlike major depressive illness, remit spontaneously with sobriety.

Dexamethasone suppression test testing of depressed alcoholics.

In order to determine the sensitivity of the dexamethasone suppression test (DST) for major depression in alcoholics, we administered this test to 27 alcoholics with major depression. Sixteen of 27 had abnormal DST results, yielding a 59% sensitivity for depression in alcoholics. When combined with previously reported specificity findings of 100%, the DST significantly (p less than 0.001) distinguished depressed from nondepressed alcoholics.

Central stimulant abuse: neurochemistry and pharmacotherapy.

This paper reviews certain clinical and neurochemical aspects of cocaine abuse. Once entrenched patterns of addiction have developed, cocaine addicts suffer progressive financial, medical, psychiatric and psychosocial deterioration that results, to some extent, from cocaine-induced neurochemical alterations in the brain. While cocaine produces euphoria through its stimulatory effect on dopamine neurons, several lines of evidence suggest that dopamine depletion occurs after chronic cocaine abuse. The dopamine neurotransmitter system is therefore a natural starting point for understanding the biology of cocaine addiction and selecting suitable adjunctive pharmacological agents. Furthermore, the dopamine depletion hypothesis implies that cocaine is "physically" addictive and provides a biological framework for understanding this disease and refining present therapeutic approaches.

Specificity of the TRH test for major depression in patients with serious cocaine abuse.

The authors administered the thyrotropin-releasing hormone (TRH) test to 17 patients with severe cocaine abuse and without major depression. The results suggest that the test is not specific for major depression when serious cocaine abuse is present.

Cocaine update: from bench to bedside.

The aim of this paper is to review and explore the psychopharmacology of cocaine from two divergent points of view--the chronic user and the laboratory. Cocaine's behavioral effects will be correlated with neurophysiological, neurochemical events, and reports by users of consequences of chronic use. These studies and reports when pieced together offer considerable promise in the development of a natural history of compulsive cocaine use. Additional neurochemical and neurophysiological research investigations are needed to allow for the development of non-addicting treatments for detoxification (à la clonidine) and prophylaxis (à la naltrexone). In the absence of these data cocaine treatment programs have been developed borrowing heavily from self help, contingency contracting and inpatient programs for working addicts.

Drug abuse and bipolar disorders.

Abuse of multiple substances can coexist in many patients who present with symptoms indistinguishable from any Bipolar Disorder. Failure to recognize and treat this coexistent substance abuse may preclude the proper management of the bipolar disorder.

Number of cortisol time-points and dexamethasone suppression test sensitivity for major depression.

Failure to suppress cortisol secretion after administration of dexamethasone has been reported to be a diagnostic marker for major depression and to have prognostic implications when repeated after antidepressant treatment. The pulsatile pattern of cortisol secretion suggested to us that increasing the number of post-dexamethasone cortisol determinations might significantly increase the sensitivity of the dexamethasone suppression test (DST) for major depression. With a conventional two-point DST (1600 h and midnight), 5% of 20 normal volunteers, 8% of 13 inpatients with non-major depressions, and 31% of 65 inpatients with primary major depression failed to suppress. With six post-dexamethasone points (0800 h, 1200 h, 1600 h, 2000 h, 2200 h, midnight), the respective percentages were 10, 15 and 44%. The additional points increased the sensitivity from 31 to 44%, mostly by identifying more major depressives with a "late escape" pattern. If a clinician is using the DST to establish a marker for major depression that can be repeated to monitor response to treatment and the likelihood of relapse, then perhaps the increased sensitivity of the six-point DST would be helpful, despite a modest decrease in specificity from 94 to 88%.

Psychopharmacologic treatment of depression.

The authors emphasize the favorable response of most patients with major depression to appropriate pharmacotherapy, and present a decision-tree approach to the pharmacotherapy of major depression. Also discussed are use of contemporary clinical nosology and neuroendocrine diagnostic tests to identify candidates for pharmacotherapy and/or ECT, use of secondary tricyclics because of their lower incidence of side-effects, monitoring plasma levels of antidepressants to achieve therapeutic levels, and potentiating tricyclic nonresponders with T3 or lithium.

The dexamethasone suppression test for major depression among opiate addicts.

The authors gave the dexamethasone suppression test (DST) to 42 opiate addicts 2 weeks after detoxification. The DST provided a sensitivity of 80% and a specificity of 93% for major depression diagnosed according to the Research Diagnostic Criteria.

Comparison of the dexamethasone suppression test and the cortisol suppression index.

Among 50 inpatients, the sensitivity and specificity of the dexamethasone suppression test (DST) were 51.7% and 85.7%, respectively. For the cortisol suppression index they were 10.3% and 91% at 8:00 a.m. and 51.7% and 57.1% at 4:00 p.m. Thus, the cortisol suppression index does not appear to be an adequate substitute for the DST.

Specificity of the DST and the TRH test for major depression in alcoholics.

The authors examined dexamethasone suppression test (DST) and thyrotropin-releasing hormone (TRH) test results in 32 chronic alcoholics without depression or hepatic disease to see if alcoholism alone might lead to positive test results. After 3 weeks of sobriety there were no DST abnormalities, but blunted TRH test results were observed in eight of the 32 alcoholics. More of the 15 patients also tested during alcohol withdrawal than of the 20 normal subjects or the 32 alcoholics without alcohol withdrawal had DST and TRH test abnormalities. When performed after 3 weeks of sobriety, the DST but not the TRH test has potential as a specific laboratory adjunct in the diagnosis of depression in alcoholics.

The TRH test and urinary MHPG in unipolar depression.

Twenty-five men and 26 women with major unipolar depression were evaluated by the TRH test and urinary MHPG excretion. A significant positive correlation between TSH response to TRH and urinary MHPG was found in the men, though not in the women. These findings suggest that at least for depressed men, central norepinephrine deficiency may be the neurobiological substrate of blunted TSH responses to TRH.

Effect of multiple time point sampling on the sensitivity of the dexamethasone suppression test.

Dexamethasone suppression test sensitivity in 188 patients was 61.6% when cortisol was measured at six time points and 48.5% when cortisol was measured twice. More patients had abnormal cortisol levels at 8:00 p.m. than at 4:00 p.m. or 10:00 p.m.