Treatment Of Depressive Illness Research Articles

Development and validation of a method to screen for co-morbid depression by non-behavioral health practitioners treating musculoskeletal pain.

BACKGROUND:Although diagnosis and treatment of depressive illness is outside the scope of practice for non-behavioral health practitioners such as occupational therapists, physical therapists, kinesiotherapists, and chiropractors, it frequently is comorbid with painful musculoskeletal disorders such as low back pain and it negatively affects outcomes, including return to work. As psychologically-informed practice becomes more widely implemented without the immediate availability of behavioral health practitioners, safe and effective methods to screen for and appropriately triage depressive illness by nonbehavioral health practitioners are necessary.OBJECTIVES:To demonstrate the efficacy and validity of a method employed by non-behavioral health practitioners to screen for and appropriately triage musculoskeletal pain patients who also are experiencing depressive illness.METHODS:As part of a previously-published psychometric research study conducted in a community-based musculoskeletal pain rehabilitation program, a method was developed for nonbehavioral health practitioners to screen for and appropriately triage patients for co-morbid depressive illness, thus providing the current opportunity to examine the effects of depressive illness on work outcomes. The first step in the two-step process involves a 22-item questionnaire, providing scores used in the second step to triage for outside consultation with behavioral health practitioners. This paper describes the screening method and its application in an observational study of the impact of depressive illness on work outcomes.RESULTS:Among 156 consecutive patients who were presenting with musculoskeletal pain disorders to an outpatient rehabilitation program, 22.3% also were identified to have co-morbid clinical depression. The screening process allowed all patients to continue in the rehabilitation program. Those who were already receiving behavioral health care were encouraged to inform care providers of their participation in the program. Those who were not receiving behavioral health care were successfully triaged to care outside of the clinic. Depressive illness was found to affect success in the program, confirming the validity of the screening process for outpatient rehabilitation program participants experiencing chronic pain.CONCLUSIONS:A simple and effective depression screening process that triages patients without interruption of musculoskeletal treatment can be employed by nonbehavioral health practitioners. Because return to work outcomes were found to be negatively affected by depressive illness, this approach has the potential to improve overall program efficacy.

Ketamine and Sleep: Bridging the Gap in the Treatment of Depressive Illness

Two articles that provide the first clear evidence for a connection between the rapid antidepressant effects of ketamine and sleep appear in this issue of Biological Psychiatry ( 1 Duncan Jr, W.C. Slonena E. Hejazi N.S. Brutsche N. Yu K.C. Park L. et al. Motor-activity markers of circadian timekeeping are related to ketamine’s rapid antidepressant properties. Biol Psychiatry. 2017; 82: 361-369 Abstract Full Text Full Text PDF PubMed Scopus (50) Google Scholar , 2 Orozco-Solis R. Montellier E. Aguilar-Amal L. Sato S. Vawter M.P. Bunney B.G. et al. A circadian genomic signature common to ketamine and sleep deprivation in the anterior cingulate cortex. Biol Psychiatry. 2017; 82: 351-360 Abstract Full Text Full Text PDF PubMed Scopus (62) Google Scholar ). These articles are timely considering the explosion of interest in providing ketamine treatment for depression, and for the fast-growing knowledge base connecting circadian rhythm to depression and other psychiatric illnesses. These articles are also important because of their relation to a fundamental problem in the understanding and treatment of depressive illness more generally. This problem (which continues despite billions spent on the development of new pharmacotherapies) is the long delay between initiation of treatment and significant improvement in the illness. This apparent requirement for an incubation of treatment before achieving meaningful benefit distinguishes psychiatric disorders in general, and depressive disorders in particular, from diseases that are not brain related. A Circadian Genomic Signature Common to Ketamine and Sleep Deprivation in the Anterior Cingulate CortexBiological PsychiatryVol. 82Issue 5PreviewConventional antidepressants usually require several weeks to achieve a full clinical response in patients with major depressive disorder, an illness associated with dysregulated circadian rhythms and a high incidence of suicidality. Two rapid-acting antidepressant strategies, low-dose ketamine (KT) and sleep deprivation (SD) therapies, dramatically reduce depressive symptoms within 24 hours in a subset of major depressive disorder patients. However, it is unknown whether they exert their actions through shared regulatory mechanisms. Full-Text PDF Motor-Activity Markers of Circadian Timekeeping Are Related to Ketamine’s Rapid Antidepressant PropertiesBiological PsychiatryVol. 82Issue 5PreviewThe rapid clinical antidepressant effects of the glutamatergic modulator ketamine may be due to its ability to restore synaptic plasticity and related effects on sleep-wake and circadian systems. Preclinical studies indicate that ketamine alters expression of circadian clock–associated molecules, and clinical studies of ketamine on plasticity-related biomarkers further suggest an association with sleep slow waves and sleep homeostasis. Full-Text PDF

Proposed model for the cultural adaptation of an Internet-based depression prevention intervention (CATCH-IT) for Arab adolescents.

Background Evidence-based Internet depression prevention intervention programs are not readily available for Arab youth, but may be effective in this group. Cultural adaptation of evidence-based Western psychotherapy is an important step toward better prevention and treatment of depressive illness in the Arab community. Project CATCH-IT is an Internet-based depression prevention intervention tool that is tailored for adolescents and young adults. Methods The PEN-3 theoretical framework was used for the cultural adaptation of Project CATCH-IT for Arab adolescents. First, a narrative review of existing research about depression in Arab nations was performed. Next, expert opinions about applicability and societal values were obtained. This model was then used to suggest relevant changes to the CATCH-IT modules. These modifications were applied to create sample webpages from the culturally adapted version of CATCH-IT for Arab youth. Results The narrative review, expert opinions and resultant PEN-3 analysis suggest that Internet-based depression interventions are effective, private and confidential. To be most effective, religious leaders and fathers should be the stakeholders approached for dissemination and adequate usage of the service. Arab themes, quotes, language and relevant stories must be incorporated. Conclusion This study sets the background for future studies and research for implementation of the Arabic version of CATCH-IT for the prevention of depression. Using the contextual information provided in this paper to make the necessary changes, huge strides can be made in providing cost-effective and accessible Internet-based interventions to Arab youth.

Association of activation syndrome with life-time hypomanic symptoms and Ghaemi criteria

ObjectiveActivation syndrome consists of 10 suicides associated symptoms, which is induced by antidepressant treatment. These are anxiety, agitation, manic episodes, sleep disruption, irritability, hostility, aggressiveness, impulsivity, akathisia and mania/hypomania. This syndrome is reported to be associated with a bipolar disorder diathesis. The aim of this study is to evaluate lifetime hypomanic symptoms with major depressive disorder, who are prescribed antidepressant medication, and to investigate whether there is a relationship between these symptoms and the development of AS.MethodsSixty consecutive outpatients with the diagnosis of major depressive disorder who were naturalistically given antidepressant treatment were examined prospectively. Patients were assessed three times; at baseline, 2 and 4 weeks later. At baseline visit, clinical characteristics of patients including Ghaemi criteria were assessed, life-time history of hypomanic symptoms were assessed with the Hypomania-Checklist-32. In all three interviews, Barnes Akathisia Rating Scale, Hamilton Rating Scale for Depression, Hamilton Anxiety Rating Scale and Young Mania Rating Scale were applied to detect the symptoms of AS. The patients who present at least one of the 10 symptoms were considered to have AS.ResultsOf the 60 patients 25(41.7%) developed AS. The most prevalent symptoms of AS are insomnia (31.7%), anxiety (25%) and irritability (15%). Significant difference was found between patients with and without AS, with regard to HCL-32 test scores. A moderate correlation between the number of AS symptoms and HCL-32 test scores were determined. AS was found to be significantly more frequent in patients with mere hypersomnia and both increased appetite and hypersomnia those without these symptoms.Disclosure of interestThe findings of this study suggest that certain features of BPS might be associated with the development of AS. Antidepressant treatment of depressive illnesses in this spectrum which are misdiagnosed as unipolar may reveal these symptoms that will complicate the current episode and destabilize the longitudinal course. For this reason, clinicians should evaluate the patients who present antidepressant induced symptoms meticulously and be careful not to overlook the characteristics of BPS.

What is the mechanism of Ketamine's rapid-onset antidepressant effect? A concise overview of the surprisingly large number of possibilities.

Abundant clinical data now confirm that ketamine produces a remarkable rapid-onset antidepressant effect - hours or days - in contrast to the delayed onset (typically weeks) of current antidepressant drugs. This surprising and revolutionary finding may lead to the development of life-saving pharmacotherapy for depressive illness by reducing the high suicide risk associated with the delayed onset of effect of current drugs. As ketamine has serious self-limiting drawbacks that restrict its widespread use for this purpose, a safer alternative is needed. Our objective is to review the proposed mechanism(s) of ketamine's rapid-onset antidepressant action for new insights into the physiological basis of depressive illness that may lead to new and novel targets for antidepressant drug discovery. A search was conducted on published literature (e.g. PubMed) and Internet sources to identify information relevant to ketamine's rapid-acting antidepressant action and, specifically, to the possible mechanism(s) of this action. Key search words included 'ketamine', 'antidepressant', 'mechanism of action', 'depression' and 'rapid acting', either individually or in combination. Information was sought that would include less well-known, as well as well-known, basic pharmacologic properties of ketamine and that identified and evaluated the several hypotheses about ketamine's mechanism of antidepressant action. Whether the mechanistic explanation for ketamine's rapid-onset antidepressant action is related to its well-known antagonism of the NMDA (N-Methyl-d-aspartate) subtype of glutamate receptor or to something else has not yet been fully elucidated. The evidence from pharmacologic, medicinal chemistry, animal model and drug-discovery sources reveals a wide variety of postulated mechanisms. The surprising discovery of ketamine's rapid-onset antidepressant effect is a game-changer for the understanding and treatment of depressive illness. There is some convergence on NMDA receptor antagonism as a likely, but to date unproven, common mechanism. The surprising number of other mechanisms, and the several novel biochemical aetiologies of depression proposed, suggests exciting new drug-discovery targets.

Inhibition of monoamine oxidase by benzoxathiolone analogues.

Inhibitors of the monoamine oxidase (MAO) enzymes are considered useful therapeutic agents, and are used in the clinic for the treatment of depressive illness and Parkinson's disease. In addition, MAO inhibitors are also under investigation for the treatment of certain cardiovascular pathologies and as possible aids to smoking cessation. In an attempt to discover novel classes of compounds that inhibit the MAOs, the current study examines the human MAO inhibitory properties of a small series of 2H-1,3-benzoxathiol-2-one analogues. The results show that the benzoxathiolones are potent MAO-B inhibitors with IC50 values ranging from 0.003 to 0.051 μM. Although the benzoxathiolones are selective for the MAO-B isoform, two compounds display good MAO-A inhibition with IC50 values of 0.189 and 0.424 μM. Dialysis studies show that a selected compound inhibits the MAOs reversibly. It may thus be concluded that the benzoxathiolone class is suitable for the design and development of MAO-B inhibitors, and that in some instances good MAO-A inhibition may also be achieved.

EPA-0169 – Effects of antidepressants on sleep architecture

Introduction Sleep disturbances are an integral part of the biological syndrome of depression and relief from this is often essential to enhance compliance with medications and psychological treatments. Anti-depressants, which are the mainstay of treatment of depressive illnesses, have varying effects on our sleep architecture. It is important for researchers and clinicians to be aware of these effects. Objectives We looked at the available literature on how antidepressants affect sleep patterns and tried to synthesize the findings in this poster. Aims The primary aim of our effort was to look at how antidepressants alter our sleeping behaviour and how they affect the different stages of sleep. Methods We tried to look at the available literature and product summary sheets of various antidepressants and have attempted to summarize how they alter our sleep architecture. Results SSRIs and TCAs have marked dose-dependent effects on REM sleep in both healthy volunteers and depressed patients, with increased REM-onset latency and decreased REM sleep. Other antidepressants have modest or minimal effects on REM sleep. The effects on sleep are most likely mediated by 5-HT1 receptors. Conclusions Most antidepressants affect sleep and the physiological patterns of different sleep stages. These effects are greatest and most consistent on rapid eye movement (REM) sleep, and tend to be in the opposite direction to the sleep abnormalities found in depression.

N-3 (omega-3) polyunsaturated Fatty acids in the pathophysiology and treatment of depression: pre-clinical evidence.

A growing literature suggests the association of low tissue levels and/or dietary intake of n-polyunsaturated fatty acids (PUFA) with depressive illnesses. Animal studies show that low tissue and/or dietary n-3 PUFAs can lead to behaviors and neurobiological effects associated with depression and can potentiate the consequences of stress, whereas higher levels have the opposite effect. These data support the involvement of n-3 PUFAs levels in the disease processes underlying depression. In addition, these pre-clinical findings indicate neurobiological mechanisms whereby n-3 PUFAs may contribute to the disease including control of serotonergic and dopaminergic function, modulation of brain-derived neurotrophic factor (BDNF) in the hippocampus, regulation of the hypothalamic-pituitary-adrenal axis, and effects on neuroinflammation. This evidence for a role for n-3 PUFA in the pathophysiology and treatment of depressive illness are reviewed. The implications of these finding for future pre-clinical research and clinical application are discussed.

Diagnosis, Pathophysiology, and Management of Mood Disorders in Pregnant and Postpartum Women

Mood disorders disproportionately affect women across the lifespan. Mood disorders in pregnancy and the postpartum period are common and have profound implications for women and their children. These include obstetric and neonatal complications, impaired mother-infant interactions, and, at the extreme, maternal suicide and infanticide. Because obstetrician-gynecologists are often the first (and sometimes the only) point of contact for young women in the health care system, familiarity with the presentation and treatment of depressive illness in the perinatal period is imperative. The goal of this review is to synthesize essential information on depressive illness in the perinatal period with a focus on its most common and severe presentations, major depressive disorder and bipolar disorder. Accurate diagnosis of unipolar major depressive disorder from bipolar disorder can facilitate the selection of the best possible treatment alternatives. Counseling may be sufficient for perinatal women who have mild to moderate depression, but women who are severely depressed are likely to require antidepressant treatment. Women with bipolar disorder are at high risk for relapse if mood stabilizer medication is discontinued, and they are vulnerable to relapse near the time of delivery. Comanagement of their care with psychiatrists will increase their chances of avoiding a recurrence of illness.

Depression and Its Correlates Among Older Adults Accessing Aging Services

: To define the prevalence and correlates of depression among older adults receiving assessments by nonmedical community-based care managers at the point of entry to care and thus prior to provision of aging services. Our long-term goal is to inform development of collaborative care models for late life depression that incorporate Aging Services Providers. : Aging Services Provider Network (ASPN) clients receiving in-home assessments were administered the Structured Clinical Interview for DSM-IV-TR (SCID) module for affective disorders and measures of depression symptom severity, alcohol use, physical health, functional status, social support, stressful life events, and religiosity. Engagement in mental healthcare was documented. : Subjects (N = 378) were primarily white (84%) and women (69%) with household incomes under $1,750/month (62%). Half lived alone (48%). Their mean age was 77 years. Thirty-one percent had clinically significant depressive symptoms and 27% met criteria for a current major depressive episode, of which 61% were being treated with medication and 25% by a mental health provider. Nearly half (47%) had experienced one or more episodes of major depression during their lives. Disability, number of medical conditions, number and severity of recent stressful life events, low social support, and low religiosity were independently associated with current major depression. : Depressive illness was common among this sample of ASPN clients. Because ASPN care managers have expertise in managing many of the problems correlated with depression, they may play a significant role in identifying, preventing, and collaborating in the treatment of depressive illnesses among community-dwelling older adults.

Diagnosis, Pathophysiology, and Management of Mood Disorders in Pregnant and Postpartum Women

Mood disorders disproportionately affect women across the lifespan. Mood disorders in pregnancy and the postpartum period are common and have profound implications for women and their children. These include obstetric and neonatal complications, impaired mother–infant interactions, and, at the extreme, maternal suicide and infanticide. Because obstetrician–gynecologists are often the first (and sometimes the only) point of contact for young women in the health care system, familiarity with the presentation and treatment of depressive illness in the perinatal period is imperative. The goal of this review is to synthesize essential information on depressive illness in the perinatal period with a focus on its most common and severe presentations, major depressive disorder and bipolar disorder. Accurate diagnosis of unipolar major depressive disorder from bipolar disorder can facilitate the selection of the best possible treatment alternatives. Counseling may be sufficient for perinatal women who have mild to moderate depression, but women who are severely depressed are likely to require antidepressant treatment. Women with bipolar disorder are at high risk for relapse if mood stabilizer medication is discontinued, and they are vulnerable to relapse near the time of delivery. Comanagement of their care with psychiatrists will increase their chances of avoiding a recurrence of illness. (Reprinted with permission from Obstet Gynecol 2011; 117:961–977)

Diagnosis, Pathophysiology, and Management of Mood Disorders in Pregnant and Postpartum Women

Mood disorders disproportionately affect women across the lifespan. Mood disorders in pregnancy and the postpartum period are common and have profound implications for women and their children. These include obstetric and neonatal complications, impaired mother-infant interactions, and, at the extreme, maternal suicide and infanticide. Because obstetrician-gynecologists are often the first (and sometimes the only) point of contact for young women in the health care system, familiarity with the presentation and treatment of depressive illness in the perinatal period is imperative. The goal of this review is to synthesize essential information on depressive illness in the perinatal period with a focus on its most common and severe presentations, major depressive disorder and bipolar disorder. Accurate diagnosis of unipolar major depressive disorder from bipolar disorder can facilitate the selection of the best possible treatment alternatives. Counseling may be sufficient for perinatal women who have mild to moderate depression, but women who are severely depressed are likely to require antidepressant treatment. Women with bipolar disorder are at high risk for relapse if mood stabilizer medication is discontinued, and they are vulnerable to relapse near the time of delivery. Comanagement of their care with psychiatrists will increase their chances of avoiding a recurrence of illness.

A psychoneuroimmunological review on cytokines involved in antidepressant treatment response

The literature exploring the role that cytokine functioning plays in the pathogenesis and treatment of depressive illness is reviewed. The review focuses on the influence of antidepressants on cytokines, and on how treatment response might be affected by genetic variants of cytokines. The authors systematically reviewed the scientific literature on the subject over the last 20 years, searching PubMed, PsychInfo, and Cochrane databases. Antidepressants modulate cytokine functioning, and these mechanisms appear to directly influence treatment outcome in depression. Antidepressants appear to normalize serum levels of major inflammatory cytokines, including interleukin (IL)-1beta, IL-6, tumor necrosis factor alpha (TNF-alpha), and interferon gamma (IFN-gamma). Antidepressants are postulated to modulate cytokine functioning through their effects on intracellular cyclic adenosyl monophosphate (cAMP), serotonin metabolism, the hypothalamo-pituitary-adrenocortical (HPA) axis or through a direct action on neurogenesis. Preliminary research shows that cytokine genotypes and functioning may be able to help predict antidepressant treatment response. Current literature demonstrates an association between antidepressant action and cytokine functioning in major depression. Improved understanding of the specific pharmacologic and pharmacogenetic mechanisms is needed. Such knowledge may serve to enhance our understanding of depression, leading to promising new directions in the pathology, nosology, and treatment of depression.

The impact of the National Institute of Clinical Excellence guidance on the use of electroconvulsive therapy in England

Electroconvulsive therapy (ECT) has been reported to have efficacy in the treatment of depressive illness, mania and catatonia (U.K. ECT Review Group, 2003; National Institute for Clinical Excellence, 2003; Scott, 2004). The Royal College of Psychiatrists in the U.K. continues to support the use of ECT within the framework of its guidance on the use of ECT (Scott, 2004) and has developed an ECT accreditation service for clincal services that use ECT. In May 2003, the National Institute of Clinical Excellence (NICE) issued a technical appraisal on the use of ECT in England (NICE, 2003). This is essentially guidance on the use of ECT which clinicians are required to follow in their clinical practice.

Perspective: Progress on the Study and Treatment of Depressive Illness

Perspective: Progress on the Study and Treatment of Depressive Illness

Issues for DSM-V: The Medical Diagnostic Model

Back to table of contents Previous article Next article EditorialFull AccessIssues for DSM-V: The Medical Diagnostic ModelMax Fink M.D.Michael A. Taylor M.D.Max Fink M.D.Search for more papers by this authorMichael A. Taylor M.D.Search for more papers by this authorPublished Online:1 Jul 2008https://doi.org/10.1176/appi.ajp.2008.08020245AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail Early in the modern psychopharmacologic era, treatment response was considered verification for a diagnosis. A well-developed response to lithium in excited patients was consistent with a diagnosis of manic depression. A response to anticonvulsants supported a diagnosis of a seizure disorder. As syndrome categories broadened in scope and became less specific (e.g., the easily met criteria for major depression), the usefulness of such responses fell and interest waned. In the 1970s, hypercortisolemia was reported among severely depressed patients but not in patients with other mental disorders. Initial observations were made in patients with melancholic depression who were so ill they were referred for electroconvulsive therapy. The abnormality disappeared with remission and reappeared with relapse. The development of a simplified dexamethasone suppression test encouraged studies. However, when the test was applied as diagnostic criterion to populations classified according to DSM-III criteria for major depression, specificity was lost and the test was precipitously discarded. Recent interest in rigorously diagnosed examples of melancholia and psychotic depression based on narrowly defined mood, motor, and vegetative symptoms suggests that hypercortisolemia may be a verifying criterion and the response to specific treatments a validating criterion (1) . Psychiatric classification has swollen into a kaleidoscope of putative disorders. It is not likely that any one rule of taxonomy will define the many entities that may be included in DSM-V. But a medical diagnostic model will define those conditions for which we already have a biological interest in their identification and, more importantly, methods of resolution.Address correspondence and reprint requests to Dr. Fink, PO Box 457, St. James, NY 11780; [email protected] attglobal.net (e-mail). Editorial accepted for publication March 2008 (doi: 10.1176/appi.ajp.2008.08020245).The authors report no competing interests.Editorials discussing other DSM-V issues can be submitted to the Journal at http: //mc.manuscriptcentral.com/appi-ajp. Submissions should not exceed 500 words.Reference1. Taylor MA, Fink M. Melancholia: The Diagnosis, Pathophysiology, and Treatment of Depressive Illness. Cambridge, UK, Cambridge University Press, 2006Google Scholar FiguresReferencesCited byDetailsCited BySchizophrenia Research, Vol. 150, No. 1Diagnostic and statistical manual of mental disorders 5: A quick glanceIndian Journal of Psychiatry, Vol. 55, No. 3 Volume 165Issue 7 July, 2008Pages 799-799THE AMERICAN JOURNAL OF PSYCHIATRY July 2008 Volume 165 Number 7 Metrics PDF download History Published online 1 July 2008 Published in print 1 July 2008

A variant of Munchausen syndrome presenting as a gynaecological emergency

A 42-year-old woman presented to the accident and emergency medicine department and was triaged to the gynaecological emergency unit with vaginal bleeding and incomplete miscarriage of 13 weeks’ gestation, which she brought in as a ‘specimen of products of conception’, following a miscarriage at home, in a plastic bag. Her last menstrual period was on 11 December 2005, which made her about 13 weeks’ gestation by date. She had three children and had had ‘three miscarriages’ previously. Her periods were regular, bleeding for 4–6 days in a regular cycle of 26–28 days. She had two ‘positive pregnancy tests’ at home but had never had an ultrasound scan before presentation. In her three previous miscarriages, there was no documented evidence of pregnancy either by a positive pregnancy test, elevated beta human chorionic gonadotrophin level, ultrasound scan findings of intrauterine pregnancy, whether viable or non-viable, or histological evidence of products of conception. She looked very distressed but her general physical examination was normal and her vital signs were within normal limits. Pelvic examination revealed minimal blood in the vagina and the cervix looked normal, but patulous. The uterus felt slightly bulky in size and mobile. An intravenous line was put up and blood taken for full blood count, C-reactive protein, grouping and saving serum, and serum beta human chorionic gonadotrophin estimation, and a pelvic ultrasound scan was arranged. The need for hospital admission was explained to complete the investigations and initiate appropriate management. She was also prescribed a course of antibiotics and analgesics. The specimen, which was in the early stage of decay, was inspected and found to be offensive. It was sent in formalin to the histopathology department for histology. The patient refused admission into the gynaecological ward and also a transvaginal ultrasound scan which had been arranged. She signed the discharge against medical advice form in spite of advice to the contrary. Further inquiry of her GP confirmed that she had had treatment for depressive illness in the past and has changed her GP frequently, making it difficult to arrange effective follow-up. The GP promised to a range psychiatric assessment as soon as practicable. It was not known at this stage that she was not actually having a miscarriage and that the purported products of conception were in fact chicken giblets.

Melancholia: The Diagnosis, Pathophysiology, and Treatment of Depressive Illnessby Michael Alan Taylor and Max Fink; New York, Cambridge University Press, 2006, 560 pages, $175

Back to table of contents Previous article Next article Book ReviewsFull AccessMelancholia: The Diagnosis, Pathophysiology, and Treatment of Depressive IllnessPatrick Runnels M.D.Patrick Runnels M.D.Search for more papers by this authorPublished Online:1 Jan 2008https://doi.org/10.1176/ps.2008.59.1.120AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail In the preface of Melancholia , the authors assert that one objective of the book is to "challenge accepted doctrines" regarding the classification and treatment of depressive illness. To this end, they don't disappoint, approaching this goal with a vigor that emanates from every section. As promised, Michael Alan Taylor and Max Fink thoroughly review all aspects of melancholia; certainly, the book accomplishes this objective effectively. However, the central thrust of the book lies in the arguments the authors present for changing how the field of psychiatry approaches depression. At the broadest level, the authors assert that melancholia, as classically defined, warrants a separate diagnostic category independent of a major depressive disorder, which they argue has been diluted by "depressive-like" illnesses that cloud clinical decision making and result in reduced quality of care. The chapters are presented as a series of small arguments concentrating on individual aspects of diagnosis, assessment, and treatment; along the way, an exhaustive body of research is compiled and analyzed in the service of these arguments. Although many assertions will feel familiar to readers, such as the contention that pharmaceutical companies have too much influence on diagnostic classification and prescribing practices, a few may be more surprising, such as the suggestion that mania might be best thought of as a melancholic variant.Though many of the book's arguments are quite persuasive, I didn't agree with every one and found myself quite opposed to a few. However, this isn't a shortcoming. On the contrary, I think efforts like this are supposed to stoke emotions and spark debate, and in that regard, I found the book to be a resounding success. The authors are, of course, biased, and the evidence they cite certainly isn't presented in a neutral way. But their methods of analysis are transparent and that allows for readers to interpret the evidence as well.A few small faults warrant attention. At times, the authors indulge in overly focused evidence review, particularly with regard to presenting differential diagnoses. Such excessive detail detracted from the overall effectiveness of the book, and some readers may choose to skim these sections. Additionally, although the authors contend that this book focuses on melancholia, they spend significant time citing evidence that questions the validity of nonmelancholic depression and the use of selective serotonin reuptake inhibitors. Although it is beyond the scope of the book, the failure to address such large issues after so provocatively raising them may leave readers somewhat unfulfilled. Despite these faults, I recommend the book without reservation. The authors targeted this book to all clinicians who are "responsible for the management of patients with mood disorders." Although I agree, I would add that Melancholia is ideally suited to residents and early-career psychiatrists who will not only gain knowledge but will also nurture the valuable skill of critically assessing mainstream psychiatry. Dr. Runnels is a public psychiatry fellow at Columbia University Medical Center and is an associate in the Office of the Medical Director, New York State Office of Mental Health. FiguresReferencesCited byDetailsCited byNone Volume 59Issue 1 January, 2008Pages 120-120PSYCHIATRIC SERVICES January 2008 Volume 59 Number 1 Metrics PDF download History Published online 1 January 2008 Published in print 1 January 2008

Melancholia: The Diagnosis, Pathophysiology, and Treatment of Depressive Illness

Melancholia: The Diagnosis, Pathophysiology, and Treatment of Depressive Illness

Melancholia: The Diagnosis, Pathophysiology, and Treatment of Depressive Illness

Melancholia: The Diagnosis, Pathophysiology, and Treatment of Depressive Illness