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Preview: Depression


Wiley Online Library : Depression

Published: 1996-01-01T00:00:00-05:00




Depression was launched in 1993 to provide a home for scientists and clinicians interested in the study and treatment of depression and related mood disorders. Depression has been remarkably successful and represents the single best source of information on the neuropsychology, pathophysiology, psychopharmacology and psychotherapy of affective disorders. The scope of articles published in Depression has included basic neuroscience, behavioral pharmacology, social and cultural aspects of depression and original research on drug and cognitive-behavioral therapies of mood disorders and related syndromes. The journal is particularly appealing to both basic and clinical neuroscientists, because of its inclusion of review articles, case reports, book reviews and, of course, research reports. The articles published in Depression present the work of the leading investigators in the field. Because the study of affective disorders and related syndromes is highly specialized, mental health professionals and scientists will always require a peer-reviewed journal on depression for the exchange of ideas and the presentation of highly technical subjects. While the fundamental necessity for a speciality journal on depression is indisputable, most of us in the mood disorders field have historical roots or a current parallel interest in the anxiety disorders. In fact, the co-morbidity between anxiety and depression has become the principal research focus of many neuroscientists and clinicians, and, more recently, clinical scholars have begun to develop specific algorithms for the treatment of patients with mixed anxiety and depression. Like Depression, the journal Anxiety (edited by Thomas W. Uhde, M.D.) is published by Wiley-Liss and has had an identical pattern of success. Similar to our readership, many individuals who read and publish articles in Anxiety have counterbalancing interests in affective disorders. Given these realities and the fact that we need to expand our coverage of topics on anxiety, alarm, fear, arousal, and startle, the former journals of Anxiety and Depression will be published as a single journal entitled, Depression and Anxiety, beginning with the next issue. Depression and Anxiety will be published eight times a year, with four issues dedicated to depression and four issues dedicated to anxiety. The Editorial Boards recognize value and respect the scientific traditions of both fields as well as the journals themselves. Therefore, the existing Editorial Boards will remain intact, operating under the auspices of a single journal entitled Depression and Anxiety. Issues of the merged journal devoted to depression and to anxiety will maintain their present formats and general style of presentation, including their own highly attractive and creative covers. Authors submitting articles on depression should continue to submit manuscripts to our Editorial Office at Emory University in Atlanta. Authors submitting articles on anxiety and related topics should submit articles to the Editorial Office of Anxiety in Columbia, Maryland. There will be no interruption in the timely publication of articles submitted to Depression, although henceforth all issues will be published as part of the merged journal of Depression and Anxiety. The publication of Depression and Anxiety represents the next logical step in the Editorial Board's pledge to advance knowledge about affective disorders and related syndromes. By activating this merger, the Editorial Board of Depression further improves its ability to provide an increased volume of high quality information on a broader range of topics. The Associate Editors, Alan F. Schatzberg, M.D. and Jay M. Weiss, Ph.D., and the Book Review Editor, Stephen Cole, M.D., as well as the Editorial Board are excited about the resultant advantages associated with this merger and we look forward to your continued participation in journal-related activities whether you are a reader, reviewer, or contributor. The Editorial Board believes you will find Depression and Anxiety to be a “must read” journal.

Venlafaxine: A novel antidepressant that has a dual mechanism of action


Major depressive disorder (MDD) is a common affective disorder that is associated with a range of psychiatric disturbances. The pathophysiology of MDD is commonly believed to involve the reduced availability of the monoamines, serotonin (5-HT) and norepinephrine (NE), the enhancement of which is also believed to mediate, at least in part, the therapeutic effects of antidepressants. The first-generation antidepressants, the tricyclic antidepressants (TCAs), provide considerable efficacy but have several limitations, including (1) delayed onset of action, (2) intolerable or distressing side effects, (3) low therapeutic index, and (4) a significant proportion of nonresponders. The second-generation antidepressants, the selective-serotonin-reuptake inhibitors (SSRIs), mitigate some of the side effects associated with the TCAs by selectively inhibiting the reuptake of 5-HT. Venlafaxine is a new antidepressant that blocks reuptake of both 5-HT and NE. It, like the SSRIs, has a relatively benign side-effect profile. In addition, it may exert a rapid onset of action, and it appears to be particularly effective in moderate-to-severe depression and in patients who have treatment-refractory depression. Depression 4:48–56 (1996). © 1997 Wiley-Liss, Inc.

Depression in patients with coronary artery disease


Depression is more prevalent in patients with coronary artery disease (CAD) than in the general elderly population. Although CAD patients with depression have higher mortality rates, depression is often not recognized and treated in these patients. We administered structured psychiatric diagnostic interviews to 99 inpatients with CAD and diagnosed 23% with a major depressive episode (MDE) by DSM-IV criteria. Severity of medical illness and family history of psychopathology were indicators for increased risk for MDE. These findings may facilitate the recognition of CAD patients at greater risk for MDE. Depression 4:57–62 (1996). © 1997 Wiley-Liss, Inc.

Six month follow-up of early-onset chronic depression


Background This study sought to characterize the morbidity and treatment behavior of 49 patients with early-onset chronic depression, 6 months after terminating treatment at a university-based psychopharmacology research clinic. Method Patients with and without early-onset chronic depression were selected to participate in a naturalistic follow-up study. Assessments were conducted blind to patients' histories. Patients' depressive symptoms, psychosocial functioning, and post-discharge treatment histories were assessed. Results After termination, the mean length of recovery for the sample was 3.6 months. When they left the clinic, 78% (38/49) were euthymic. At follow-up, 37% (14/38) of these had relapsed; while 45% (17/38) remained in remission for 6 months. During the follow-up period, 47% of the patients were on antidepressants. Sixty-three percent of the patients who relapsed, or were depressed when they left the clinic, did not enter treatment, 50% of whom cited insufficient resources as the primary reason for not receiving care. Conclusions After leaving a depression research clinic, a substantial portion of patients with early-onset chronic depression remained recovered during a 6-month period, but financial impediments prevented a majority of those who did poorly from entering treatment. Depression 4:63–67 (1996). © 1997 Wiley-Liss, Inc.

Depressive symptoms: Associations with health perceptions and health behaviors


The association of depressive symptoms with health behaviors and perceptions was determined for 876 patients seeing family physicians. Correlational analyses revealed stress, pain, and overall health status were moderately related to depression for males and females. Smoking was positively related to depressive symptoms in women (r = .19, P <.001), and drinking was inversely related to depressive symptoms in men (r = −.16, P <.01). Multiple regression analyses indicated stress, poor health, smoking, and drinking were significant predictors of depressive symptoms in women; stress, poor health, and drinking were significant in men. Health perceptions appear to be better predictors of depressive symptoms than reported health behaviors. Depression 4:68–72 (1996). © 1997 Wiley-Liss, Inc.

Lack of association between thyroid and pineal responses to antidepressant treatment


With antidepressant treatment for major depression there are decreases in thyroid hormone levels and increases in pineal function. We have conducted a study to examine whether there is a relationship between pineal and thyroid hormone measures as well as between hormone measures and response to treatment in patients treated with desipramine. Measures of thyroid activity included thyroxine, triiodothyronine, T3 resin uptake, and TSH. Pineal function was determined by measurement of 6-suphatoxymelatonin in three consecutive 8 hour pools. Hormone measures as well as Hamilton depression scores were obtained prior to treatment and at the end of 5 weeks of treatment. As in previous studies, thyroid measures decreased, pineal activity increased, and Hamilton scores decreased significantly with treatment. No correlations were found between these measures, suggesting that if there is a relationship between them it is not a direct one. Depression 4:73–76 (1996). © 1997 Wiley-Liss, Inc.

Do patients use marijuana as an antidepressant?


Several lines of evidence suggest that cannabis may have antidepressant effects. However, methodologic limitations in available studies make the results difficult to interpret. We review this literature and present five cases in which the evidence seems particularly clear that marijuana produced a direct antidepressant effect. If true, these observations argue that many patients may use marijuana to “self-treat” depressive symptoms. Depression 4:77–80 (1996). © 1997 Wiley-Liss, Inc.

Effects of self-generated sad mood on regional cerebral activity: A PET study in normal subjects


This study investigated the cerebral regions modulated by self-generated sad mood in normal subjects. Eleven healthy men experienced a temporary sad mood by recalling sad personal memories. Two control states were used for comparison: a resting condition, and a condition involving the recall of affectively neutral personal events. Regional cerebral blood flow (rCBF) images were obtained using [15O]-H2O Positron Emission Tomography. A statistical comparison of the images during negative mood and neutral recall conditions revealed that sad mood was associated with a decrease in rCBF in the left dorsolateral prefrontal, left medial prefrontal, and left temporal cortex; no increase in activity was noted in this comparison. Our results are consistent with the noted left prefrontal decrease in metabolism found in depressed patients through a variety of methodologies; however, our results contrast with findings of increased left or bilateral prefrontal activity in transient induced negative mood states reported for women (George et al., 1995, Am J Psychiatry 152:341–341) and for mixed-gender (Pardo et al., 1993, Am J Psychiatry 150:713–719) subject groups. The study brings to light a number of methodological issues, including the crucial importance of the baseline condition used for the isolation of the emotional components of a given task. Depression 4:81–88 (1996). © 1997 Wiley-Liss, Inc.

An empirical study of the psychodynamics of suicide: A preliminary report


Preliminary results from a study of psychodynamic constructs are presented based on data from inpatients following a suicide attempt. The study examines the association between four psychodynamic constructs, severity of suicidal intent, and severity of depressive symptomatology in a sample of hospitalized suicide attempters. Higher levels of suicidal intent were associated with less differentiated self and object representations and less emotional investment in relationships. More severe depressive symptoms in suicide attempters were correlated with more self-targeted anger; less eternally directed anger, higher levels of shame and guilt, more affectively negative views of relationships, greater use of maladaptive and self-sacrificing defenses, and more impaired reality testing. These findings offer some preliminary empirical support for the validity of psychodynamic theories of suicidal behavior. Depression 4:89–91 (1996). © 1997 Wiley-Liss, Inc.

Rapid cycling triggered by pindolol augmentation of paroxetine, but not with desipramine


A treatment-resistant depressed patient developed bipolar rapid cycling in response to pindolol augmentation of paroxetine, after failing to respond in any fashion to pindolol added to desipramine. The rapid cycling initially faded, but recurred after the pindolol dose was increased (in combination with paroxetine) in an attempt to treat a relapse into depression. Her differential development of rapid cycling with pindolol in combination with the SSRI is in keeping with the theory that pindolol augmentation operates via a serotonergic mechanism. Depression 4:92–94 (1996). © 1997 Wiley-Liss, Inc.

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