Psychiatric Annals

Published by Slack
Online ISSN: 0048-5713
Publications
Article
Obesity and depression are two major public health problems among adolescents. Both obesity and depression are very prevalent and associated with numerous health complications, including hypertension, coronary heart disease, and increased mortality.1 Because they both carry a risk for cardiovascular disease, a possible association between depression and obesity has been assumed and studied.2 Several evidence-based studies have shown that obese teens have a higher incidence of mental health problems such as depression, anxiety, and poor self-esteem than nonobese teens.3 A reasonable conclusion is that obesity should predict depression, but the findings are not clear.4 In reality, few studies have found that obesity predicted depression over time, thus it has been proposed that instead of looking at the basic main effects of obesity predicting depression, it might be more practical to examine the specific processes or experiences by which obesity might lead to depression among adolescents so that specific interventions can be targeted.5 This article summarizes data on the role of mediating and moderating variables associated with obesity and depression among adolescents. This literature review also examines the thoughts and experiences of obese adolescents that facilitate the development of depressive symptoms.
 
Article
The objective of this study is to discuss contemporary and historical factors affecting racial health disparities in psychiatric clinical care, evaluate black cultural mistrust of the mental healthcare system, identify institutional and clinician-level approaches for increasing clinical care use by blacks for adolescent depression. Regarding blacks and psychiatric clinical care in particular, the following discussion is presented to elucidate sociocultural (ie, nonfinancial) barriers to treatment, the unique aspects of shame and stigma that blacks associate with treatment, and black cultural mistrust of the mental health system. The focus of clinical care in this article is adolescent depression. The findings on adolescent depression and perceptions of clinical care and research among blacks raise a number of concerns, including the effects of a limited evidence base for treating depression in these youth and perceptions of clinical research and care by blacks for youth with psychiatric illness. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
 
Article
Psychiatry is a profession defined and guided by well-established norms dating back to the Hippocratic Oath and carefully delineated by the standards of modern biomedical ethics and professionalism. Key principles, such as beneficence (confidentiality), autonomy (informed consent), nonmaleficence, and justice provide bases for clinical judgment in specific contexts. Commercialism in health care introduces potential conflicts for the professional, whose primary allegiances are to the patient and those served. Several new challenges are faced by psychiatrists and other professionals in the twenty-first century. These include telemedicine, electronic health records, and social networks/social media.
 
Results of WECare Data Analysis MRM MI without Amount of Tx Received in Imputation Model Pattern Mixture Model MI with Amount of Tx Received in Imputation Model Parameter Est SE P val Est SE P val Est SE P val Est SE P val 
Article
Longitudinal designs in psychiatric research have many benefits, including the ability to measure the course of a disease over time. However, measuring participants repeatedly over time also leads to repeated opportunities for missing data, either through failure to answer certain items, missed assessments, or permanent withdrawal from the study. To avoid bias and loss of information, one should take missing values into account in the analysis. Several popular ways that are now being used to handle missing data, such as the last observation carried forward (LOCF), often lead to incorrect analyses. We discuss a number of these popular but unprincipled methods and describe modern approaches to classifying and analyzing data with missing values. We illustrate these approaches using data from the WECare study, a longitudinal randomized treatment study of low income women with depression.
 
Article
Increasingly, multiple outcomes are collected in order to characterize treatment effectiveness or to evaluate risk factors. These outcomes tend to be correlated because they are measuring related quantities in the same individuals. While the analysis of outcomes measured in the same scale (commensurate outcomes) can be undertaken with standard statistical methods, outcomes measured in different scales (non-commensurate outcomes), such as mixed binary and continuous outcomes, present more difficult challenges.In this paper we contrast some statistical approaches to analyze non-commensurate multiple outcomes. We discuss the advantages of a multivariate method for the analysis of non-commensurate outcomes including situations of missing data. A real data example from a clinical trial, comparing different treatments for depression in low-income women, is used to illustrate the differences between the statistical approaches.
 
Article
The etiology and pathophysiology of body dysmorphic disorder (BDD), as with most psychiatric disorders, is likely complex. Because research is limited, the causative and contributory factors to the development of BDD are unclear. Yet there is emerging evidence from research studies of various factors that may contribute to the development and maintenance of BDD symptoms. This review of the etiology and pathophysiology of BDD explores what has been elucidated thus far from research on developmental, psychosocial, cognitive and behavioral, neuropsychological, and neurobiological (visual processing, neuroanatomical, genetic, and neurochemical) factors. We explore “submodels” of BDD within these domains, and we synthesize these to generate an overarching, yet preliminary, model of the etiological and pathophysiological processes that appear to contribute to the development and maintenance of BDD. This model involves a context of likely biological and genetic susceptibility upon which adverse life events interact with cognitive distortions and subsequent learned behavior to result in BDD symptoms. Given the limited research base, this model – while reflecting available research evidence – serves primarily a heuristic function. We hope nonetheless that this model informs clinicians’ thinking about how to understand patients with BDD.
 
Article
Bereavement is a ubiquitous part of the human condition. Almost no person makes it through his or her life without having to cope with the loss of a loved one several different times. The loss of a parent, child, or grandparent can be very distressing. For many, the most devastating loss is that of their spouse or partner, which usually occurs during later life. More than 800,000 older Americans are widowed every year. Apart from the severe emotional strain of the loss of a loved one, there are profound changes in lifestyle and status, often accompanied by reductions in financial security, perceived personal safety, and freedom of action. Thus, late-life spousal bereavement (LLSB) comprises one of the major impacts of bereavement on society. Losses of family members or close friends can also be very traumatic, depending upon the nature of the death and/or the vulnerability of the individual. Most people experiencing grief from bereavement find that there is a lessening of the intensity of the grief as time progresses. For a majority, five emotional and cognitive stages of grief arise, peak, and dissipate within 6 months.1 However, those who continue to show elevated cognitive and affective symptoms 6 months postloss at are at higher risks for poor health outcomes, and require further intervention. For instance, complicated grief (CG), also referred to as prolonged grief disorder or traumatic grief, has recently gained acceptance in individuals for whom the usual time-limited course of emotional recovery from the loss event does not occur, and the associated emotional distress and functional impairments persist. Six-month postloss, a score of > 25 on the Inventory of Complicated Grief (ICG)2 is used to indicate CG. The literature on sleep and bereavement is limited. This review focuses on two areas for which there are some findings to report, namely LLSB and CG. For LLSB, we will include the loss of a life partner of the same generation, whether or not the two people were formally married. One can regard LLSB and CG as bereavement situations for which sleep disruptions are likely to be maximal.
 
Article
In summary, the risk factors of sleep disruptions in cancer patients are multifactorial. Savard and Morin7 summarized insomnia-related factors in cancer into three categories: (1 predisposing factors that increase the individual’s general vulnerability to develop insomnia, such as hyper-arousability, being female, aging, and a personal and a familial history of insomnia; 2) precipitating factors that trigger the onset of sleep disturbances, such as the cancer itself, cancer-related emotional impact and functional loss, and cancer-related treatments and symptoms such as pain, and delirium; and 3) perpetuating factors that contribute to the maintenance of sleep disturbance over time, such as maladaptive sleep behaviors and faulty beliefs and attitudes about sleep. Based on the research findings, it is likely that sleep disruptions in cancer patients, particularly insomnia, are more likely comorbid with cancer and with other cancer-related symptoms, rather than secondary to cancer treatments and other cancer-related symptoms, such as fatigue, pain, and depression.
 
Article
The purpose of these reflections on a very sensitive subject is primarily exploratory and provocative. The author does not lay down a new code of ethics for the medical profession or for society in general. But widespread discussion of these matters is essential and this discussion should take place not only in medical circles but among all professional people concerned with human health and behavior as well. Eventually there will emerge a new and more humane consensus about the meaning of life and death and how these issues are to be dealt with in this society.
 
Article
Depression is a common phenomenon among patients with alcohol or drug dependence, as is evident to any practitioner working with these patients. Numerous studies have documented high rates of depressive disorders among patients seeking treatment for substance use disorders.1 Community surveys have consistently found elevated rates of major depression and dysthymia among patients with alcohol or drug dependence.2–6 Further, current major depression has been associated with worse clinical outcome among substance-dependent patients.1,7,8 The data are less clean on the prognostic implications of a past depression or elevated depressive symptoms without identification of a depressive disorder. These epidemiological data suggest that a co-occurring depressive disorder is important and warrants clinical attention. Yet the management of this co-occurring depression has been a source of confusion and considerable controversy. The data are also clear that in many cases depressive symptoms resolve within days or weeks after a patient becomes abstinent or enters an effective treatment modality such as methadone maintenance.9–13 Thus, one school of thought holds that such depression is mostly a consequence of ongoing addiction — effects of substance intoxication, or withdrawal, or perhaps the stress of the addicted lifestyle. The appropriate treatment is treatment of the addiction to get the patient abstinent and into recovery, after which the depression should resolve. Another school holds that depression should be treated and that such treatment might help patients achieve abstinence, perhaps because the addiction is partly driven by “self-medication” of the symptoms of depression. This leads to the problem of how to determine who to treat among actively using outpatients with substance abuse and co-occuring depression. Should clinicians treat any elevation of depression symptoms? Or should the treat only depressive syndromes, such as major depression, accompanied by a convincing past history of independent depression? If a depression syndrome (eg, major depression) persists after a period of abstinence, then virtually all clinicians would acknowledge that at some point it be declared an independent disorder and treated as such with antidepressant medication or psychotherapy. But what length of abstinence is needed to make this determination? Two decades ago, many experts might have recommended that a depression should persist for 6 months into abstinence. The Diagnostic and Statistical Manual of Mental Disorders, 4th edition, published in 1994, curtailed this period to 1 month.14 Seeking evidence to address these questions, numerous placebo-controlled clinical trials have now been conducted testing antidepressant medications among substance-dependent populations meeting various depression criteria. The results, if simply tallied up, are decidedly mixed, with a number of studies suggesting that antidepressant medication is effective among substance-dependent patients with depression and a similar number of studies showing no beneficial effect. This is where a quantitative review of the literature, namely a meta-analysis, can be helpful. In this article, we will review meta-analyses of the literature on antidepressant treatment among substance-dependent patients and show how these analyses help to explain discrepancies between positive and negative studies, thereby informing clinical recommendations.
 
Article
Psychiatrists are increasingly called upon to care for individuals with cognitive, emotional, and behavioral disturbances after TBI, especially in settings serving military service personnel and Veterans. In both the early and late post-injury periods, cognitive impairments contribute to disability among persons with TBI and are potentially substantial sources of suffering for persons with TBI and their families. In this article, the differential diagnosis, evaluation, and management of posttraumatic cognitive complaints is reviewed. The importance of pre-treatment evaluation as well as consideration of non-cognitive contributors to cognitive problems and functional limitations is emphasized first. The course of recovery after TBI, framed as a progression through posttraumatic encephalopathy, is reviewed next and used to anchor the evaluation and treatment of posttraumatic cognitive impairments in relation to injury severity as well as time post-injury. Finally, pharmacologic and rehabilitative interventions that may facilitate cognitive and functional recovery at each stage of posttraumatic encephalopathy are presented.
 
Article
In the last decade, the number of publications in psychiatric genetics has nearly tripled but little attention has been paid to the role of genetic factors in the etiology of posttraumatic stress disorder (PTSD). The present review summarizes the current state of genetic research on PTSD. First, we outline information regarding genetic influences provided by family investigations and by twin studies. Second, we propose the fear-conditioning model of PTSD as a framework for the nomination of candidate genes that may be related to the disorder. Third, we review lines of evidence from three neurobiological systems involved in fear conditioning, and we summarize published investigations of genetic variants studied in association with PTSD in these three systems. Finally, we review gene-by-environment interaction research, a promising novel approach to genetic research in PTSD.
 
Article
Obtaining informed consent and following a standard of care are of importance in monitoring antipsychotic medications and also can assist in the early detection of tardive dyskinesia in the elderly.
 
Article
Posttraumatic stress disorder (PTSD) is a common psychiatric disorder in populations exposed to trauma, and it is among the most functionally-impairing, similar in scope to that observed in mood disorders. Recent years have seen many treatment studies assessing efficacy of diverse pharmacotherapies for PTSD. This article reviews the established, evidence-based pharmacotherapeutic treatments for PTSD and highlights current recommendations and controversial areas. The article primarily focuses on published randomized clinical trials that tested overall symptom reduction in PTSD compared to placebo. We also briefly review efforts to target particular symptoms commonly associated with PTSD (eg, sleep disturbance; psychotic symptoms) and at preventing PTSD among populations recently exposed to trauma. Where appropriate, recommendations are made for use of particular agents as first-line pharmacotherapies. To date, there are no validated sensitive and specific biomarkers of PTSD that can aid in diagnosis, treatment selection, or monitoring of clinical progress. Notable biological findings in PTSD1 include derangements in the two main branches of the stress response system, the noradrenergic/sympathetic brain systems and the hypothalamic-pituitary-adrenal (HPA) axis;2 increased cerebrospinal fluid concentrations of corticotropin-releasing factor (CRF);3,4 reduced volume of the hippocampus;5–7 functional differences in responding of fear system brain regions, such as hyperactivation of the amygdala and hypoactivation of the prefrontal cortex;8–10 sleep disturbances;11 measures of hyperarousal in response to stimuli and of delayed habituation to loud noises;12 and evidence for impaired conditioned fear extinction recall.13,14 Such findings have firmly grounded the psychopathology of PTSD in neurobiological dysfunctions, thereby suggesting routes of pharmacotherapeutic interventions.15 Agents that enhance serotonergic neurotransmission, such as serotonin selective reuptake inhibitors (SSRIs), appear to attenuate several of the prominent symptoms of the PTSD. However, randomized clinical trials (RCTs) published to date have, at best, demonstrated limited efficacy for the constellation of symptoms that make up PTSD.16,17 In fact, effect sizes (Cohen’s d statistic) from the best pharmacotherapy RCTs have been relatively small, prompting the United Kingdom’s National Institute for Clinical Excellence to recommend that medication treatments not be used as routine first-line treatments in preference to a trial of a trauma-focused psychological therapy.18 Yet the overall conclusion of a recent meta-analysis of existing RCTs in PTSD conducted by the Cochrane Collaboration was that medication treatments were superior to placebo in reducing the severity of PTSD symptom clusters as well as comorbid depression and disability.19 Therefore, both combination psychotherapy and pharmacotherapy and psychotherapy alone should be considered as first line approaches to PTSD while pharmacotherapy alone is generally not recommended, except in the circumstance when proven efficacious psychotherapies are not available.
 
Article
While much psychiatric research is based on randomized controlled trials (RCTs), where patients are randomly assigned to treatments, sometimes RCTs are not feasible. This paper describes propensity score approaches, which are increasingly used for estimating treatment effects in non-experimental settings. The primary goal of propensity score methods is to create sets of treated and comparison subjects who look as similar as possible, in essence replicating a randomized experiment, at least with respect to observed patient characteristics. A study to estimate the metabolic effects of antipsychotic medication in a sample of Florida Medicaid beneficiaries with schizophrenia illustrates methods.
 
Top-cited authors
Bessel A van der Kolk
  • Trauma Research Foundation
Joseph Spinazzola
  • Foundation Trust
Richard Kagan
  • Training Programs on Traumatic Stress
Marylene Cloitre
  • National Center for PTSD
Alexandra Cook
  • The Trauma Center at JRI