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The purpose of the present study was to assess the validity of the Beck Depression Inventory (BDI), the MMPI Depression scale (MMPI-D), and the Rorschach Depression Index (DEPI) in measuring adolescent depression. Retroactive charts of 118 hospitalized adolescents were divided into depressed (n=66) and nondepressed (n=52) groups, based on the psychiatric diagnosis. Results indicated significant differences between the means of the two groups on the BDI (p<0.00001) and the MMPI-D scale (p<0.0001), establishing concurrent validity for these measures of depression. Correlation coefficients among the three measures of depression indicated a significant relationship between the BDI and the MMPI-D scale (p<0.01), again supporting the concurrent validity of these instruments. Predictive utility was determined for each of the three instruments individually and in combination, with results indicating that the BDI and MMPI-D scales alone and in combination significantly discriminated depressed from nondepressed adolescents. The MMPI-D scale alone was the most accurate measure in classifying the participants into their respective groups. The DEPI was not established as a valid predictor of adolescent depression.
Sixty-eight depressive inpatients were subdivided into an acutely suicidal (n = 34) and a non-suicidal control group (n = 34) by means of item I of the Beck Depression Inventory (BDI). The two groups were matched in age and sex. Electrodermal activity (SCL, SFL, SCR, habituation speed) and heart rate (HR) were recorded in a standard habituation experiment. In self-assessment scales, depression (BDI), trait anxiety (STAI-X1) and bodily complaints (B-L') were evaluated. Assuming a correlation between EDA and serotonergic transmission, we expected clear evidence of serotonergic dysfunction in the acutely suicidal group according to the hypothesis of a deficiency in serotonergic transmission in acutely suicidal depressives. Acutely suicidal depressives showed significantly higher depression and anxiety symptoms as well as more physical complaints (compared to the controls). As for the EDA experiments, SCLs and amplitudes of the first EDRs were significantly reduced in the acutely suicidal depressives (in comparison with the controls), whereas their heart rate was increased. Although the subjects of both groups were not selected regarding suicidality or suicidal attempts in their case history before admission to the depression ward but only for suicidality at the time of the experiment, these results are similar to those of depressive patients we examined during inpatient treatment and who later committed violent suicide. Further research on the mechanisms of central serotonergic regulation are necessary to shed light on the question whether acute serotonergic dysfunctions or outlasting deficiencies significantly contribute to results as found in this study.
In contrast to its inhibitory role in mature neurons, GABA can exert excitatory actions in developing neurons, including mediation of increases in cytosolic Ca2+. Modulation of this excitatory activity has not been studied previously. We used Ca2+ digital imaging with Fura-2 to test the hypothesis that neuropeptide Y (NPY) would depress GABA-mediated Ca2+ rises in neurons cultured from the developing suprachiasmatic nucleus (SCN). SCN neurons were chosen as a model system for this study because SCN neurons are primarily GABAergic, they express high levels of NPY and GABA receptors, and functionally, NPY causes profound phase-shifts in SCN-generated circadian rhythms. Vigorous GABA-mediated Ca2+ activity was found in young SCN neurons that were maintained in vitro for 4-14 d. NPY showed a dose-dependent rapid depression of the amplitude of Ca2+ rises generated by GABA released from presynaptic SCN axons. NPY exerted a long-term depression of cytosolic CA2+ in the majority of neurons tested, which lasted more than 1 hr after NPY washout. The magnitude of the NPY depression was dose-dependent. NPY did not affect Ca2+ levels when GABAA receptor activity was blocked by bicuculline; however, when bicuculline and NPY were withdrawn from the perfusion solution, the subsequent CA2+ rise was either significantly reduced or completely absent, suggesting that the NPY receptor was activated in the absence of elevated intracellular Ca2+ and GABAA receptor activity, and that the latent effect of NPY was revealed only after depolarizing GABA stimulation was renewed. Pretreating neurons with pertussis toxin greatly reduced the ability of NPY to depress GABAergic Ca2+ rises, suggesting that the NPY modulation of the GABA activity was based largely on a mechanism involving pertussis toxin-sensitive Gi/Go proteins. NPY receptor stimulation depressed (< 30%) postsynaptic Ca2+ rises evoked by GABA (20 microM) application in the presence of tetrodotoxin (TTX). The effects of NPY were mimicked by the NPY Y1 receptor agonist [Pro34,Leu31] NPY and the Y2 receptor agonist NPY 13-36 and by peptide YY (PYY). Together, our data suggest that the Y1 and Y2 type NPY receptors act both presynaptically and postsynaptically to depress GABA-mediated Ca2+ rises. If related mechanisms exist in peptide modulation of inhibitory GABA activity in mature neurons, this could underlie long-term changes in the behavior of neurons of the SCN necessary for phase-shifting the circadian clock by NPY, NPY also modulated GABA responses in neuroendocrine neurons from the hypothalamic arcuate nucleus. NPY thus can play an important role in evoking long-term depression of GABA-mediated Ca2+ activity in these developing neurons, allowing NPY-secreting cells to modulate the effects of GABA on neurite outgrowth, gene expression, and physiological stimulation. This is the first example of such a cellular memory: that is, long-term Ca2+ depression based on modulation of depolarizing GABA activity.
A multivariate classification technique was used to examine whether depressive symptoms and symptoms frequently associated with depressive disorders would cluster into recognizable syndromes that parallel traditional DSM-III psychiatric diagnoses. An analysis was made of all respondents in the Epidemiologic Catchment Area (ECA) project of the Piedmont region of North Carolina who reported suffering from depressive symptoms (n = 406) at the second wave of the ECA study. The analysis identified five profiles of symptoms that adequately described the interrelationships of the symptoms as reported in the population. One profile included a set of symptoms nearly identical to the symptoms associated with the DSM-III classification of major depression. Other depressive syndromes emerged and included a premenstrual syndrome among younger women and a mixed anxiety/depression syndrome. The existence of these other depressive syndromes may explain the present discrepancy in the epidemiologic literature between a high prevalence of depressive symptoms and a low prevalence of traditional depressive diagnoses in community populations.
OBJECTIVES: To examine the frequency and distribution of depressive symptoms among subjects with binge eating disorder (BED), bulimia nervosa (BN), and major depression. METHODS: This study examined depressive symptoms from the Hamilton Depression Scale in 122 BED, 142 BN, and 200 major depression subjects using discriminant function analysis. RESULTS: All three groups differed significantly on the Hamilton Depression Scale totals with major depressive disorder (MDD) subjects having the highest and BED subjects the lowest totals. Eighteen items differentiated MDD from the eating disorder groups. Three items-gastrointestinal (GI) somatic symptoms, paranoid symptoms, and obsessional symptoms-distinguished BED and BN. In each case these symptoms were more common in BN subjects. DISCUSSION: This study attempted to differentiate BN from BED on a basis other than eating behavior. The results provide limited support for the hypothesis that BN and BED can be distinguished on the basis of depressive symptoms.
The specific symptoms of depression associated with increased mortality in the depressed elderly are poorly known. The aim of this paper is to analyse the individual depressive symptoms measured by the Zung Self Rated Depression Scale (ZSDS) and the Hamilton Rating Scale for Depression (HRSD) in association with mortality among depressed elderly subjects. The population consisted of 169 depressed (DSM-III criteria) aged (65+ years) persons from a Finnish epidemiological research project. The follow-up for deaths continued for about 6 years. When age, sex, smoking, physical health and functional abilities were taken into account, dissatisfaction, weight loss and gastrointestinal symptoms (anorexia and constipation) predicted mortality together with high age and poor physical health. Weight loss was related to an increased risk of death, specifically in the depressed. Dissatisfaction and gastrointestinal symptoms were more general markers of increased mortality.
This paper reports on the regional prevalence of symptoms of depression and clinical depression (current major depressive episodes) in Greece in the years 1978 and 1984. Prevalence rates were estimated from two extensive, nationwide cross-sectional home surveys on psychosocial issues and health, carried out in four geographical areas: the Greater Athens area, the Greater Thessaloniki area, the rest of the urban areas and rural areas. The methodology used, the sampling procedure and the screening instrument (The Center for Epidemiologic Studies-Depression Scale) were the same in both surveys. Within the 6-year period a substantial increase in the prevalence of symptoms of depression in all geographic areas was observed, with the Athenian respondents expressing a higher number of symptoms of depression than their counterparts from the other areas. The prevalence of current major depressive episodes, according to specific criteria matched with criteria from the DSM III R, was increased in 1984 in Athens and in the rural areas only. We suggest that economic instability between 1978 and 1984 probably contributed to the changes in the rates of depressive disorders.
A multicentre study on the epidemiology of perinatal depression was conducted among Japanese women expecting the first baby (N = 290). The incidence rate of the onset of the DSM-III-R Major Depressive Episode during pregnancy (antenatal depression) and within 3 months after delivery (postnatal depression) were 5.6% and 5.0%, respectively. Women with antenatal depression were characterised by young age and negative attitude towards the current pregnancy, whereas women with postnatal depression were characterised by poor accommodation, dissatisfaction with sex of the newborn baby and with the emotional undermining. Antenatal depression was a major risk factor for postnatal depression.
In a study of 144 women, mainly self-designated PMS sufferers, the premenstrual depression experienced was, apart from its shorter duration, quantitatively and qualitatively similar to major depressive disorder for a substantial proportion of subjects. The associations with previous history of depression were complex: the severity of premenstrual depression was related to previous history of postnatal depression, whereas its duration (i.e., whether it persisted through longer) was related to a history of treatment with antidepressants. Two independent dimensions are proposed. (i) A menstrual cycle-related factor which in vulnerable women can results in severe and disabling premenstrual dysphoria, and which may be aetiologically related to a subgroup of postnatal depression. (ii) In a minority of women a more general propensity for depressive illness evidence as a tendency for any premenstrual depression to be prolonged.
This study aimed to validate and determine an appropriate cut-off score on the Thai Edinburgh Postnatal Depression Scale (EPDS) as a screen for postpartum depression. A prospective cohort of postpartum women at 6-8 weeks were tested using the EPDS and clinically interviewed by psychiatrists to establish a DSM-IV diagnosis of major or minor depressions in a university hospital in Southern Thailand. Of 351 postpartum women interviewed, 38 postpartum women met the criteria for depressive disorders, major depression in four women (1%) and minor depressive disorder in 34 women (10%). The area under the curve was 0.84 (95% confidence interval 0.76-0.91). Using an EPDS cut-off sum score of 6/7, major and/or minor depression was detected with a sensitivity of 74%, specificity of 74%, positive predictive value of 26% and negative predictive value of 95%. When the cut-off score was higher, the sensitivity was lower but the specificity was higher. The Thai version of the EPDS is a valid self-report instrument and is useful in Thailand where no other screening instrument for postpartum depression is available.
Patients with chronic medical illness have a high prevalence of major depressive illness. Major depression may decrease the ability to habituate to the aversive symptoms of chronic medical illness, such as pain. The progressive decrements in function associated with many chronic medical illnesses may cause depression, and depression is associated with additive functional impairment. Depression is also associated with an approximately 50% increase in medical costs of chronic medical illness, even after controlling for severity of physical illness. Increasing evidence suggests that both depressive symptoms and major depression may be associated with increased morbidity and mortality from such illnesses as diabetes and heart disease. The adverse effect of major depression on health habits, such as smoking, diet, over-eating, and sedentary lifestyle, its maladaptive effect on adherence to medical regimens, as well as direct adverse physiologic effects (i.e., decreased heart rate variability, increased adhesiveness of platelets) may explain this association with increased morbidity and mortality.
Traditionally, both stress and depression have been associated with impaired immune function and increased susceptibility to infectious and neoplastic disease. However over the last number of years a large body of evidence suggests that major depression is associated with signs of immunological activation. Moreover it has been suggested that cytokine hypersecretion may be involved in the aetiology of depressive disorders. The present article reviews the evidence from both clinical and experimental studies which implicates immunological activation and particularly hypersecretion of cytokines in the onset and maintenance of depressive illness. Both clinical and experimental studies indicate that stress and depression are associated with increased circulating concentrations of cytokines such as IL-1beta, IL-6 and gamma-IFN and positive acute phase proteins, and hyperactivity of the HPA-axis. In addition, it has been reported that immunological activation induces "stress-like" behavioural and neurochemical changes in laboratory animals. Although for many years it has been suggested that stress acts a predisposing factor to depressive illness, the precise mechanisms by which stress-induced depressive symptoms occur are not fully understood. Nevertheless, behavioural changes due to stress have often been explained in terms of changes in neurotransmitter function in the brain. In the present article increased cytokine secretion is implicated as a mechanism whereby stress can induce depression.
It is pragmatically important to know the comparative prognoses of bipolar, unipolar and subthreshold depressions after they present to clinical attention. Previous studies focusing on bipolar and/or unipolar depressions have questionable generalizability because of overrepresentation of inpatients and/or refractory patients, and no study has yet focused on the length of subthreshold depression. The Group for Longitudinal Affective Disorders Study (GLADS) in Japan is conducting a prospective, serial follow-up study of broadly defined mood disorder patients, who had not received treatment for their index episode before study entry. The median time to recovery for bipolar depression was 2.0 months (95%CI: 0.9-3.1), that for unipolar depression 3.0 (2.5-3.6), and that for subthreshold depression 3.2 (0-12.3). Survival analyses revealed no statistically significant difference among the three. Neither was the total time unwell significantly different among the three: on average, these patients were symptomatic with two or more significant affective symptoms for 9.5 (8.0-10.9) months out of the initial 24 months of follow-up. The bipolar depressed patients tended to present with graver functional impairment at intake, but thereafter there was no statistically significant difference in the global functioning of these three diagnostic subgroups. In our sample, patients with depressive disorder not otherwise specified appeared to suffer both symptomatologically and functionally as much as patients with major mood disorders.
The tripartite model of depression and anxiety suggests that anhedonia represents a relatively specific marker of depression. A strong version of this view is that anhedonic symptoms would particularly characterize depressed patients, even when compared to another diagnostic group-schizophrenic patients-for whom anhedonic symptoms represent a well-studied feature. This prediction was tested among 102 VA psychiatric inpatients (95 men), ages 21-72 (M=43.56; S.D.=8.47), all of whom received diagnoses of either major depression (n=50) or schizophrenia (n=52) based on structured diagnostic interviews. As predicted, patients with major depression scored significantly higher on the anhedonic symptoms scale of the Beck Depression Inventory (BDI) than did patients with schizophrenia. However, there was no difference between the two groups on the BDI total score or the BDI non-anhedonic symptoms score. Consistent with the tripartite model, anhedonic symptoms were more related to depressive vs. schizophrenic diagnostic status, whereas non-anhedonic depressive symptoms were not. Within the study's limitations, results were interpreted as relatively strong support for the validity and extension of the tripartite model.