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Biomedical subjects

J Greden

Publications and source records attributed to J Greden.

10 recordsLinked to original sources
PubMed1996

Electroconvulsive treatment in adolescents with pharmacotherapy-refractory depression.

The effectiveness and safety of ECT in pharmacotherapy-refractory depression was examined in 11 hospitalized adolescents (ages 16.3 +/- 1.7 years, 10 females) with a primary DSM-III-R diagnosis of mood disorder, which had failed to respond to three or more adequate trials of antidepressant pharmacotherapy. After a thorough diagnostic evaluation, patients received a course of ECT involving 11.2 +/- 2.0 (range 8-15) administrations. ECT was commenced with bilateral treatment in 2 adolescents and nondominant right electrode placement in 9 patients; 5 of the 9 patients were subsequently changed to bilateral treatment. All 11 patients improved to a clinically significant degree. Significant improvements were noted in scores on the Children Depression Rating Scale-Revised (CDSR-R) and the Global Assessment of Functioning Scale (GAF) (p < 0.05). Euthymia, defined as CDRS-R score < or = 40, was achieved by 64% (7/11) of patients. The Mini-Mental State Examination showed no significant decline in cognitive functioning. Neuropsychological testing completed in 5 subjects both before ECT and 1-5 days after the last treatment, indicated a significant decline in attention, concentration, and long-term memory search. Minor side effects, experienced within the first 12 hours of treatment, were headache (80% of patients) and nausea/vomiting (64%). The potentially serious complication of tardive seizure (after full recovery of consciousness) occurred in 1 adolescent. Prolonged seizures (> 2.5 minutes) were noted in 7 of the 11 patients (9.6% of the 135 ECT administrations). Pending further research on ECT in youth, it is recommended that ECT should only be administered to youth in hospital settings, that all regularly administered psychotropic medications (including antidepressants) be discontinued before ECT and restarted after the final administration of ECT, and that physicians be aware that 12 treatments are usually sufficient, but that 15 treatments may occasionally be necessary for treating depressed adolescents. With the understanding that scientific evaluation of ECT in youth is lacking, it appears that ECT can be an effective and relatively safe treatment for depressed adolescents who have failed to respond to antidepressant pharmacotherapy.

Antidepressive Agents↗
PubMed1993

Multiple HPA profiles in endogenous depression: effect of age and sex on cortisol and beta-endorphin.

We have previously shown that a number of depressed patients demonstrated a failure to suppress corticotrophic secretion, as measured by beta-Endorphin/beta-Lipotropin (beta-End/beta-LPH levels), following dexamethasone challenge. The current study is an extension and replication of these findings, as well as an analysis of some of the biological variables which may contribute to the variance in beta-End/beta-LPH nonsuppression. We continue to observe a high rate of beta-End/beta-LPH nonsuppression in depressed patients following dexamethasone; this escape at the pituitary level is even observed in a number of patients who demonstrate normal cortisol suppression. Advancing age, particularly in women, led to higher baseline cortisol, lower baseline beta-End/beta-LPH, and a greater likelihood of being a nonsuppressor on one or both measures.

Adrenocorticotropic Hormone↗
PubMed1993

Immune function in alcoholism: a controlled study.

Several studies have shown an increased risk for infection and cancer in alcoholic patients. The mechanisms for such observations remain largely unknown. In an effort to investigate the possibility of immunological dysfunction in alcoholism, we studied three immune parameters in 47 hospitalized chronic alcoholic patients and 47 age- and sex-matched normal controls. The immune measures were: (1) lymphocyte phenotyping, with estimates of percentages of T cells, B cells, T helpers, T suppressors, natural killer (NK) cells, and cells carrying the activation markers IL2R1 and I2; (2) NK cell activity; and (3) lymphokine-activated killer cell activity. Results indicate a significant increase in the IL2R and I2 lymphocyte markers in alcoholic patients compared with matched controls. We also found a nonsignificant trend for a decrease in the percentage of suppressor T cells in the alcoholic group, as well as a trend for a negative correlation between the percentage of T suppressor cells and age. There were no significant differences in either NK or lymphokine-activated killer cell activities between the two groups. Furthermore, there were no significant associations between duration and intensity of alcohol consumption and any of the immune measures. These results suggest subtle alterations in immune regulation in alcoholic patients that cannot be explained solely on the basis of duration and/or amount of alcohol consumed.

Adult↗
PubMed1986

beta-Endorphin/beta-lipotropin immunoreactivity in endogenous depression. Effect of dexamethasone.

This study addresses the question of whether pituitary peptides (ie, beta-endorphin) show regulatory disruption in endogenous depression and, if so, does it co-occur in the same subjects who show cortisol dysregulation. Endogenously depressed patients and psychiatric controls from three centers were evaluated, when not taking medications, and studied for plasma cortisol and beta-endorphin levels. Plasma samples were taken at four time points over one hour, on the basal day, and 16 hours after 1 mg of dexamethasone. From 33% to 69% of the endogenous patients were abnormal in their postdexamethasone cortisol levels, and from 50% to 69% were abnormal on postdexamethasone beta-endorphin values (vs 0% and 8%, respectively, for controls). When endogenous subjects were evaluated for abnormality on both cortisol and beta-endorphin, after dexamethasone, it was found that the two measures of hypothalamic-pituitary-adrenal dysfunction did not necessarily co-vary. In fact when having either abnormal beta-endorphin or cortisol levels (or both) was used as a biological marker a larger number of the endogenous patients were detected than with either measure alone. Our conclusions are as follows: Plasma beta-endorphin shows a circadian rhythm similar to that seen with corticotropin (ACTH) and is suppressable by dexamethasone. In many endogenous patients plasma beta-endorphin levels escape from dexamethasone suppression. Many of these subjects are not cortisol escapers. When abnormality of either the beta-endorphin or cortisol is considered it is clear that both levels of the hypothalamic-pituitary-adrenal axis can be dysregulated in endogenous depression.

Adolescent↗
PubMed1986

Depression, urinary free cortisol excretion and lymphocyte function.

An impairment in lymphocyte response to mitogen stimulation, a correlate of cell-mediated immunity, has been reported in patients with depressive illness. To investigate whether such impairment in lymphocyte function is related to excessive secretion of cortisol, an immunosuppressive hormone, we compared mitogen-induced lymphocyte proliferation in three groups of subjects: depressed patients with elevated 24-hour urinary free cortisol (UFC) excretion; depressed patients with normal UFC excretion; and normal controls. Depressed patients in both groups showed significant reductions in lymphocyte mitogenic activity, in comparison with the normal controls, but the two depressive groups did not significantly differ from each other in their lymphocytic responses to any of the mitogens used. Furthermore, no significant correlations were found, within depressed patients, between UFC excretion and lymphocyte mitogenic responses. Depression is therefore associated with an impairment in lymphocyte function that cannot be explained solely on the basis of increased cortisol secretion.

Depressive Disorder↗
PubMed1983

Impaired lymphocyte function in depressive illness.

Mood states and immunity may be related. To investigate the immune status of patients with primary depressive illness, we compared in-vitro lymphocytic responses to three different mitogens in 26 drug-free depressed patients and 20 normal controls of comparable age and sex. We observed a generalized and marked decrease in the lymphocyte mitogenic activity among the depressive group. This defect in lymphocyte function may be indicative of an impairment in cell-mediated immunity in patients with primary depressive illness.

Adult↗