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Showing papers in "Archives of General Psychiatry in 1998"


Journal ArticleDOI
TL;DR: The risk of PTSD associated with a representative sample of traumas is less than previously estimated, and sudden unexpected death of a loved one is a far more important cause of PTSD in the community, accounting for nearly one third of PTSD cases.
Abstract: Methods: A representative sample of 2181 persons in the Detroit area aged 18 to 45 years were interviewed by telephone to assess the lifetime history of traumatic events and PTSD, according to DSM-IV. Posttraumatic stress disorder was assessed with respect to a randomly selected trauma from the list of traumas reported by each respondent, using a modified version of the Diagnostic Interview Schedule, Version IV, and the World Health Organization Composite International Diagnostic Interview. Results: The conditional risk of PTSD following exposure to trauma was 9.2%. The highest risk of PTSD was associated with assaultive violence (20.9%). The trauma most often reported as the precipitating event among persons with PTSD (31% of all PTSD cases) was sudden unexpected death of a loved one, an event experienced by 60% of the sample, and with a moderate risk of PTSD (14.3%). Women were at higher risk of PTSD than men, controlling for type of trauma. Conclusions: The risk of PTSD associated with a representative sample of traumas is less than previously estimated. Previous studies have overestimated the conditional risk of PTSD by focusing on the worst events the respondents had ever experienced. Although recent research has focused on combat, rape, and other assaultive violence as causes of PTSD, sudden unexpected death of a loved one is a far more important cause of PTSD in the community, accounting for nearly one third of PTSD cases. Arch Gen Psychiatry. 1998;55:626-632

2,357 citations


Journal ArticleDOI
TL;DR: Anxiety or depressive disorder during adolescence confers a strong risk for recurrent anxiety or depressive disorders during early adulthood, and most anxiety and depressive disorders in young adults may be preceded by anxiety or depression in adolescence.
Abstract: Background Various studies find relationships among anxiety and depressive disorders of adolescence and adulthood. This study prospectively examines the magnitude of longitudinal associations between adolescent and adult anxiety or depressive disorders. Methods An epidemiologically selected sample of 776 young people living in upstate New York received DSM -based psychiatric assessments in 1983, 1985, and 1992 using structured interviews. The magnitude of the association between adolescent and adult anxiety or depressive disorders was quantified using odds ratios generated from logistic regression analyses and from a set of latent Markov analyses. We focus on longitudinal associations among narrowly defined DSM anxiety or depressive disorders. Results In simple logistic models, adolescent anxiety or depressive disorders predicted an approximate 2- to 3−fold increased risk for adulthood anxiety or depressive disorders. There was evidence of specificity in the course of simple and social phobia but less specificity in the course of other disorders. Results from the analyses using latent variables suggested that while most adolescent disorders were no longer present in young adulthood, most adult disorders were preceded by adolescent disorders. Conclusions An anxiety or depressive disorder during adolescence confers a strong risk for recurrent anxiety or depressive disorders during early adulthood. Most anxiety and depressive disorders in young adults may be preceded by anxiety or depression in adolescence.

1,665 citations


Journal ArticleDOI
TL;DR: Treatment of depression in patients with CVD improves their dysphoria and other signs and symptoms of depression, improves quality of life, and perhaps even increases longevity.
Abstract: This article reviews the burgeoning literature on the relationship of mood disorders and heart disease. Major depression and depressive symptoms, although commonly encountered in medical populations, are frequently underdiagnosed and undertreated in patients with cardiovascular disease (CVD). This is of particular importance because several studies have shown depression and its associated symptoms to be a major risk factor for both the development of CVD and death after an index myocardial infarction. This review of the extant literature is derived from MEDLINE searches (1966-1997) using the search terms "major depression," "psychiatry," "cardiovascular disease," and "pathophysiology." Studies investigating pathophysiological alterations related to CVD in depressed patients are reviewed. The few studies on treatment of depression in patients with CVD are also described. Treatment of depression in patients with CVD improves their dysphoria and other signs and symptoms of depression, improves quality of life, and perhaps even increases longevity. Recommendations for future research are proposed.

1,567 citations


Journal ArticleDOI
TL;DR: The prevalence of community violence by people discharged from acute psychiatric facilities varies considerably according to diagnosis and, particularly, co-occurring substance abuse diagnosis or symptoms.
Abstract: Background The public perception that mental disorder is strongly associated with violence drives both legal policy (eg, civil commitment) and social practice (eg, stigma) toward people with mental disorders. This study describes and characterizes the prevalence of community violence in a sample of people discharged from acute psychiatric facilities at 3 sites. At one site, a comparison group of other residents in the same neighborhoods was also assessed. Methods We enrolled 1136 male and female patients with mental disorders between the ages of 18 and 40 years in a study that monitored violence to others every 10 weeks during their first year after discharge from the hospital. Patient self-reports were augmented by reports from collateral informants and by police and hospital records. The comparison group consisted of 519 people living in the neighborhoods in which the patients resided after hospital discharge. They were interviewed once about violence in the past 10 weeks. Results There was no significant difference between the prevalence of violence by patients without symptoms of substance abuse and the prevalence of violence by others living in the same neighborhoods who were also without symptoms of substance abuse. Substance abuse symptoms significantly raised the rate of violence in both the patient and the comparison groups, and a higher portion of patients than of others in their neighborhoods reported symptoms of substance abuse. Violence in both patient and comparison groups was most frequently targeted at family members and friends, and most often took place at home. Conclusions "Discharged mental patients" do not form a homogeneous group in relation to violence in the community. The prevalence of community violence by people discharged from acute psychiatric facilities varies considerably according to diagnosis and, particularly, co-occurring substance abuse diagnosis or symptoms.

1,372 citations


Journal ArticleDOI
TL;DR: A meta-analysis of all available EE and outcome studies in schizophrenia confirmed that EE is a significant and robust predictor of relapse in schizophrenia and demonstrated that the EE-relapse relationship was strongest for patients with more chronic schizophrenic illness.
Abstract: Background Expressed emotion (EE) is a measure of the family environment that has been demonstrated to be a reliable psychosocial predictor of relapse in schizophrenia. However, in recent years some prominent nonreplications of the EE-relapse relationship have been published. To more fully address the question of the predictive validity of EE, we conducted a meta-analysis of all available EE and outcome studies in schizophrenia. We also examined the predictive validity of the EE construct for mood disorders and eating disorders. Methods An extensive literature search revealed 27 studies of the EE-outcome relationship in schizophrenia. Using meta-analytic procedures, we combined the findings of these investigations to provide an estimate of the effect size associated with the EE-relapse relationship. We also used meta-analysis to provide estimates of the effect sizes associated with EE for mood and eating disorders. Results The results confirmed that EE is a significant and robust predictor of relapse in schizophrenia. Additional analyses demonstrated that the EE-relapse relationship was strongest for patients with more chronic schizophrenic illness. Interestingly, although the EE construct is most closely associated with research in schizophrenia, the mean effect sizes for EE for both mood disorders and eating disorders were significantly higher than the mean effect size for schizophrenia. Conclusion These findings highlight the importance of EE in the understanding and prevention of relapse in a broad range of psychopathological conditions.

1,229 citations


Journal ArticleDOI
TL;DR: Mexican Americans had lower rates of lifetime psychiatric disorders compared with rates reported for the US population by the National Comorbidity Survey, and psychiatric morbidity among Mexican Americans is primarily influenced by cultural variance rather than socioeconomic status or urban vs rural residence.
Abstract: Background The Mexican American Prevalence and Services Survey presents lifetime prevalence rates for 12 DSM-III-R psychiatric disorders in a sample of 3012 adults of Mexican origin by place of residence and nativity, and compares these results with those of population surveys conducted in the United States and Mexico. Methods The stratified random sample included noninstitutionalized persons aged 18 to 59 years of Mexican origin, who were residents of Fresno County, California. Psychiatric disorders were assessed using a modified version of the World Health Organization Composite International Diagnostic Interview in face-to-face interviews. Results Mexican immigrants had lifetime rates similar to those of Mexican citizens, while rates for Mexican Americans were similar to those of the national population of the United States. This difference is attributable to a prevalence rate for any disorder among immigrants of 24.9%, compared with 48.1% among US-born respondents. A higher prevalence for any disorder was reported in urban (35.7%) compared with town (32.1%) or rural (29.8%) areas. Multivariate analyses showed an adjusted effect of country of birth, but not of urban residence. Conclusions Despite very low education and income levels, Mexican Americans had lower rates of lifetime psychiatric disorders compared with rates reported for the US population by the National Comorbidity Survey. Psychiatric morbidity among Mexican Americans is primarily influenced by cultural variance rather than socioeconomic status or urban vs rural residence.

922 citations


Journal ArticleDOI
TL;DR: The long-term weekly course of unipolar MDD is dominated by prolonged symptomatic chronicity, and MDD, MinD, and SSD symptom levels commonly alternate over time in the same patients as a symptomatic continuum of illness activity of a single clinical disease.
Abstract: Background Investigations of unipolar major depressive disorder (MDD) have focused primarily on major depressive episode remission/recovery and relapse/recurrence This is the first prospective, naturalistic, long-term study of the weekly symptomatic course of MDD Methods The weekly depressive symptoms of 431 patients with MDD seeking treatment at 5 academic centers were divided into 4 levels of severity: (1) depressive symptoms at the threshold for MDD; (2) depressive symptoms at the threshold for minor depressive or dysthymic disorder (MinD); (3) subsyndromal or subthreshold depressive symptoms (SSDs), below the thresholds for MinD and MDD; and (4) no depressive symptoms The percentage of weeks at each level, number of changes in symptom level, and medication status were analyzed overall and for 3 subgroups defined by mood disorder history Results Patients were symptomatically ill in 59% of weeks Symptom levels changed frequently (18/y), and 9 of 10 patients spent weeks at 3 or 4 different levels during follow-up The MinD (27%) and SSD (17%) symptom levels were more common than the MDD (15%) symptom level Patients with double depression and recurrent depression had more chronic symptoms than patients with their first lifetime major depressive episode (72% and 65%, respectively, vs 46% of follow-up weeks) Conclusion The long-term weekly course of unipolar MDD is dominated by prolonged symptomatic chronicity Combined MinD and SSD level symptoms were about 3 times more common (43%) than MDD level symptoms (15%) The symptomatic course is dynamic and changeable, and MDD, MinD, and SSD symptom levels commonly alternate over time in the same patients as a symptomatic continuum of illness activity of a single clinical disease

756 citations


Journal ArticleDOI
TL;DR: Schizophrenia is associated with a bilateral volumetric reduction of the hippocampus and probably of the amygdala as well, which reinforces the importance of the medial temporal region in schizophrenia and is consistent with frequently reported memory deficits in these patients.
Abstract: Background Although many quantitative magnetic resonance imaging studies have found significant volume reductions in the hippocampi of patients with schizophrenia compared with those of normal control subjects, others have not. Therefore, the issue of hippocampal volume differences associated with schizophrenia remains in question. Methods Two meta-analyses were conducted to reduce the potential effects of sampling error and methodological differences in data acquisition and analysis. Eighteen studies with a total patient number of 522 and a total control number of 426 met the initial selection criteria. Results Meta-analysis 1 yielded mean effect sizes of 0.37 (P Conclusions Schizophrenia is associated with a bilateral volumetric reduction of the hippocampus and probably of the amygdala as well. These findings reinforce the importance of the medial temporal region in schizophrenia and are consistent with frequently reported memory deficits in these patients. Future quantitative magnetic resonance imaging studies evaluating the hippocampal volume should measure the hippocampus and amygdala separately and compare the volumetric reduction in these structures to that observed in other gray matter areas.

713 citations


Journal ArticleDOI
TL;DR: Elevation in risk of drug disorders among the relatives of probands with drug disorders across a wide range of specific substances, including opioids, cocaine, cannabis, and alcohol, which is largely independent from the familial aggregation of both alcoholism and antisocial personality disorder.
Abstract: Background: There is increasing evidence that substance use disorders are familial and that genetic factors explain a substantial degree of their familial aggregation. To perform a controlled family study of probands with several different predominant drugs of abuse, including opioids, cocaine, cannabis, and/or alcohol. Methods: The subjects for the present study included 231 probands with dependence on opioids, cocaine, cannabis, and/or alcohol and 61 control probands, and their 1267 adult first-degree relatives. Diagnostic estimates were based on semistructured diagnostic interviews and/or structured family history interviews regarding each proband, spouse, and adult first-degree relative. The interview data were reviewed blindly and independently by clinicians with extensive experience in the evaluation and treatment of substance use disorders. Results: There was an 8-fold increased risk of drug disorders among the relatives of probands with drug disorders across a wide range of specific substances, including opioids, cocaine, cannabis, and alcohol, which is largely independent from the familial aggregation of both alcoholism and antisocial personality disorder. There was also evidence of specificity of familial aggregation of the predominant drug of abuse. Conclusions: Elevation in risk of this magnitude places a family history of drug disorder as one of the most potent risk factors for the development of drug disorders. These results suggest that there may be risk factors that are specific to particular classes of drugs as well as risk factors that underlie substance disorders in general.

700 citations


Journal ArticleDOI
TL;DR: In this article, the authors found that the acceleration of incidence rates for AD and dementia slows down with the increase in age, although there is no sign of a decline in the incidence rates themselves.
Abstract: Background Prevalence studies on dementia and Alzheimer disease (AD) have reported a positive association with age. However, the trend of the association in the oldest-old categories has been the subject of discussion. The relationship between sex and AD has been inconsistent with these studies. Prevalence rates are influenced by the survival and disease incidence. Incidence rates provide a better measure of disease risk. Methods English-language articles identified through a MEDLINE search on "incidence dementia" and "incidence Alzheimer's disease" were examined and references from identified articles were reviewed. Population-based studies using personal interviews, standard clinical diagnosis criteria ( DSM-III for dementia, National Institute of Neurological and Communicative Disorders and Stroke–Alzheimer's Disease and Related Disorder Association for AD) and reporting age-specific incidence rates were included in the meta-analysis. Data from the selected studies were extracted and verified. Mixed-effect models were used in the meta-analysis to accommodate the heterogeneity of the studies. Results Incident dementia and AD are associated with a significant quadratic age effect indicating that the increase in incidence rates slows down with the increase in age, although there is no sign of a decline in the incidence rates themselves. The odds ratios for women to develop incidence of dementia and AD relative to men are 1.18 (95% confidence interval, 0.95-1.46) and 1.56 (95% confidence interval, 1.16-2.10), respectively. Conclusions The acceleration of incidence rates for AD and dementia slows down with the increase in age, although we find no evidence of a rate decline. Women are at higher risk of developing AD than men.

696 citations


Journal ArticleDOI
TL;DR: Evidence is found for a shared or common vulnerability factor that underlies the abuse of marijuana, sedatives, stimulants, heroin or opiates, and psychedelics that is influenced by genetic, family environmental, and nonfamily environmental factors.
Abstract: Background Previous research has demonstrated genetic and environmental influences on abuse of individual substances, but there is less known about how these factors may influence the co-occurrence of abuse of different illicit drugs. Methods We studied 3372 male twin pairs from the Vietnam Era Twin Registry. They were interviewed using the Diagnostic Interview Schedule, Version III, Revised to investigate the extent to which the abuse of different categories of drugs occurs together within an individual, as well as the possibility that genetic and environmental factors are responsible for observed co-occurrence. Co-occurrence was quantified using odds ratios and conditional probabilities. Multivariate biometrical modeling analyses were used to assess genetic and environmental influences on co-occurrence. Results Abusing any category of drug was associated with a marked increase in the probability of abusing every other category of drugs. We found evidence for a shared or common vulnerability factor that underlies the abuse of marijuana, sedatives, stimulants, heroin or opiates, and psychedelics. This shared vulnerability is influenced by genetic, family environmental, and nonfamily environmental factors, but not every drug is influenced to the same extent by the shared vulnerability factor. Marijuana, more than other drugs, was influenced by family environmental factors. Each category of drug, except psychedelics, had genetic influences unique to itself (ie, not shared with other drug categories). Heroin had larger genetic influences unique to itself than did any other drug. Conclusion There are genetically and environmentally determined characteristics that comprise a shared or common vulnerability to abuse a range of illicit drugs.

Journal ArticleDOI
TL;DR: The observed influences from major depression to subsequent daily smoking and smoking to major depression support the plausibility of shared etiologies.
Abstract: Background Epidemiologic studies have reported an association between major depression and smoking. This prospective study examines the role of depression in smoking progression and cessation, and the role of smoking in first-onset major depression. Methods Data are from a 5-year longitudinal epidemiologic study of 1007 young adults. Incidence and odds ratios (ORs) are based on the prospective data. Hazards ratios are based on the combined lifetime data and estimated in Cox proportional hazards models with time-dependent covariates. Results Based on the prospective data, history of major depression at baseline increased significantly the risk for progression to daily smoking (OR, 3.0; 95% confidence interval, 1.1-8.2), but did not decrease significantly smokers' rate of quitting (OR, 0.8; 95% confidence interval, 0.4-1.6). History of daily smoking at baseline increased significantly the risk for major depression (OR, 1.9; 95% confidence interval, 1.1-3.4). These estimates were reduced somewhat when history of early (ie, before age 15 years) conduct problems was controlled. Estimates based on lifetime data were consistent with these results. Conclusions The observed influences from major depression to subsequent daily smoking and smoking to major depression support the plausibility of shared etiologies. Separate causal mechanisms in each direction might also operate, including self-medication of depressed mood as a factor in smoking progression and neuropharmacologic effects of nicotine and other smoke substances on neurotransmitter systems linked to depression.

Journal ArticleDOI
TL;DR: Relatives of anorexic and bulimic probands had increased risk of clinically subthreshold forms of an eating disorder, major depressive disorder, and obsessive-compulsive disorder and obsessional personality traits may be a specific familial risk factor for anorexia nervosa.
Abstract: Background We used contemporary family-epidemiological methods to examine patterns of comorbidity and familial aggregation of psychiatric disorders for anorexia and bulimia nervosa. Methods Direct interviews and blind best-estimate diagnostic procedures were used with diagnostically "pure" groups of probands with eating disorders and a matched control group. Lifetime prevalence rates of eating disorders, mood disorders, substance use disorders, anxiety disorders, and selected personality disorders were determined in female probands with restricting anorexia nervosa (n=26) or bulimia nervosa (n=47), control women (n=44), and first-degree biological relatives (n=460). Results Relatives of anorexic and bulimic probands had increased risk of clinically subthreshold forms of an eating disorder, major depressive disorder, and obsessive-compulsive disorder. Familial aggregation of major depressive disorder and obsessive-compulsive disorder was independent of that of anorexia nervosa and bulimia nervosa. These relatives also had increased risk of other anxiety disorders, but the mode of familial transmission was not clear-cut. The risk of substance dependence was elevated among relatives of bulimic probands compared with relatives of anorexic probands, and familial aggregation was independent of that of bulimia nervosa. The risk of obsessive-compulsive personality disorder was elevated only among relatives of anorexic probands, and there was evidence that these 2 disorders may have shared familial risk factors. Conclusions There may be a common familial vulnerability for anorexia nervosa and bulimia nervosa. Major depressive disorder, obsessive-compulsive disorder, and substance dependence are not likely to share a common cause with eating disorders. However, obsessional personality traits may be a specific familial risk factor for anorexia nervosa.

Journal ArticleDOI
TL;DR: In this paper, a controlled study, 87 patients with posttraumatic stress disorder of at least 6 months' duration were randomly assigned to have 10 sessions of 1 of 4 treatments: prolonged exposure (imaginal and live) alone; cognitive restructuring alone; combined prolonged exposure and cognitive restructuring; or relaxation without prolonged exposure or cognitive restructuring.
Abstract: Background Unanswered questions from controlled studies of posttraumatic stress disorder concern the value of cognitive restructuring alone without prolonged exposure therapy and whether its combination with prolonged exposure is enhancing. Methods In a controlled study, 87 patients with posttraumatic stress disorder of at least 6 months' duration were randomly assigned to have 10 sessions of 1 of 4 treatments: prolonged exposure (imaginal and live) alone; cognitive restructuring alone; combined prolonged exposure and cognitive restructuring; or relaxation without prolonged exposure or cognitive restructuring. Results Integrity of audiotaped treatment sessions was satisfactory when rated by an assessor unaware of the treatment assignment. Seventy-seven patients completed treatment. The pattern of results was similar regardless of rater, statistical method, measure, occasion, and therapist. Exposure and cognitive restructuring, singly or combined, improved posttraumatic stress disorder markedly on a broad front. Gains continued to 6-month follow-up and were significantly greater than the moderate improvement from relaxation. Conclusion Both prolonged exposure and cognitive restructuring were each therapeutic on their own, were not mutually enhancing when combined, and were each superior to relaxation.

Journal ArticleDOI
TL;DR: The results support the following conclusions: first, the stable structure of traits across clinical and nonclinical samples is consistent with dimensional representations of personality disorders, and second, the higher-order traits of personality disorder strongly resemble dimensions of normal personality.
Abstract: Background The evidence suggests that personality traits are hierarchically organized with more specific or lower-order traits combining to form more generalized higher-order traits. Agreement exists across studies regarding the lower-order traits that delineate personality disorder but not the higher-order traits. This study seeks to identify the higher-order structure of personality disorder by examining the phenotypic and genetic structures underlying lower-order traits. Methods Eighteen lower-order traits were assessed using the Dimensional Assessment of Personality Disorder–Basic Questionnaire in samples of 656 personality disordered patients, 939 general population subjects, and a volunteer sample of 686 twin pairs. Results Principal components analysis yielded 4 components, labeled Emotional Dysregulation, Dissocial Behavior, Inhibitedness, and Compulsivity, that were similar across the 3 samples. Multivariate genetic analyses also yielded 4 genetic and environmental factors that were remarkably similar to the phenotypic factors. Analysis of the residual heritability of the lower-order traits when the effects of the higher-order factors were removed revealed a substantial residual heritable component for 12 of the 18 traits. Conclusions The results support the following conclusions. First, the stable structure of traits across clinical and nonclinical samples is consistent with dimensional representations of personality disorders. Second, the higher-order traits of personality disorder strongly resemble dimensions of normal personality. This implies that a dimensional classification should be compatible with normative personality. Third, the residual heritability of the lower-order traits suggests that the personality phenotypes are based on a large number of specific genetic components.

Journal ArticleDOI
TL;DR: In this article, the effects of mild stress exposure on higher cognitive function in monkeys and the role of dopaminergic mechanisms in the stress response were examined on a spatial working memory task (delayed response) dependent on the prefrontal cortical (PFC) cognitive deficits.
Abstract: Background Stress can exacerbate a number of psychiatric disorders, many of which are associated with prefrontal cortical (PFC) cognitive deficits. Biochemical studies demonstrate that mild stress preferentially increases dopamine turnover in the PFC. Our study examined the effects of acute, mild stress exposure on higher cognitive function in monkeys and the role of dopaminergic mechanisms in the stress response. Methods The effects of loud (105-dB) noise stress were examined on a spatial working memory task (delayed response) dependent on the PFC, and on a reference memory task with similar motor and motivational demands (visual pattern discrimination) dependent on the inferior temporal cortex. The role of dopamine mechanisms was tested by challenging the stress response with agents that decrease dopamine receptor stimulation. Results Exposure to noise stress significantly impaired delayed-response performance. Stress did not impair performance on "0-second" delay control trials and did not alter visual pattern discrimination performance, which is consistent with impaired PFC cognitive function rather than nonspecific changes in performance. Stress-induced deficits in delayed-response performance were ameliorated by pretreatment with drugs that block dopamine receptors (haloperidol, SCH 23390) or reduce stress-induced PFC dopamine turnover in rodents (clonidine, naloxone hydrochloride). Conclusions These results indicate that stress impairs PFC cognitive function through a hyperdopaminergic mechanism. Stress may take the PFC "off-line" to allow more habitual responses mediated by posterior cortical and subcortical structures to regulate behavior. This mechanism may have survival value, but may often be maladaptive in human society, contributing to the vulnerability of the PFC in many neuropsychiatric disorders.

Journal ArticleDOI
TL;DR: Alcohol, marijuana, and cocaine dependence and habitual smoking are all familial, and there is evidence of both common and specific addictive factors transmitted in families.
Abstract: Background Alcoholism and substance dependence frequently co-occur. Accordingly, we evaluated the familial transmission of alcohol, marijuana, and cocaine dependence and habitual smoking in the Collaborative Study on the Genetics of Alcoholism. Methods Subjects (n=1212) who met criteria for both DSM-III-R alcohol dependence and Feighner definite alcoholism and their siblings (n=2755) were recruited for study. A comparison sample was also recruited (probands, n=217; siblings, n=254). Subjects were interviewed with the Semi-Structured Assessment for the Genetics of Alcoholism. The familial aggregation of drug dependence and habitual smoking in siblings of alcohol-dependent and non–alcohol-dependent probands was measured by means of the Cox proportional hazards model. Results Rates of alcohol, marijuana, and cocaine dependence and habitual smoking were increased in siblings of alcohol-dependent probands compared with siblings of controls. For siblings of alcohol-dependent probands, 49.3% to 50.1% of brothers and 22.4% to 25.0% of sisters were alcohol dependent (lifetime diagnosis), but this elevated risk was not further increased by comorbid substance dependence in probands. Siblings of marijuana-dependent probands had an elevated risk of developing marijuana dependence (relative risk [RR], 1.78) and siblings of cocaine-dependent probands had an elevated risk of developing cocaine dependence (RR, 1.71). There was a similar finding for habitual smoking (RR, 1.77 in siblings of habitual-smoking probands). Conclusions Alcohol, marijuana, and cocaine dependence and habitual smoking are all familial, and there is evidence of both common and specific addictive factors transmitted in families. This specificity suggests independent causative factors in the development of each type of substance dependence.

Journal ArticleDOI
TL;DR: The health policy implications of discrepant and/or high prevalence rates for determining treatment need in the context of managed care definitions of "medical necessity" are discussed.
Abstract: During the past 2 decades, psychiatric epidemiological studies have contributed a rapidly growing body of scientific knowledge on the scope and risk factors associated with mental disorders in communities. Technological advances in diagnostic criteria specificity and community case-identification interview methods, which made such progress feasible, now face new challenges. Standardized methods are needed to reduce apparent discrepancies in prevalence rates between similar population surveys and to differentiate clinically important disorders in need of treatment from less severe syndromes. Reports of some significant differences in mental disorder rates from 2 large community surveys conducted in the United States—the Epidemiologic Catchment Area study and the National Comorbidity Survey—provide the basis for examining the stability of methods in this field. We discuss the health policy implications of discrepant and/or high prevalence rates for determining treatment need in the context of managed care definitions of "medical necessity."

Journal ArticleDOI
TL;DR: Binge eating disorder appears to be associated with exposure to risk factors for psychiatric disorder and for obesity, and pre-morbid perfectionism, negative self-evaluation, and vulnerability to obesity appear especially to characterize those in whom bulimia nervosa subsequently develops.
Abstract: Background Many risk factors have been implicated for eating disorders, although little is known about those for binge eating disorder. Methods A community-based, case-control design was used to compare 52 women with binge eating disorder, 104 without an eating disorder, 102 with other psychiatric disorders, and 102 with bulimia nervosa. Results The main risk factors identified from the comparison of subjects with binge eating disorder with healthy control subjects were certain adverse childhood experiences, parental depression, vulnerability to obesity, and repeated exposure to negative comments about shape, weight, and eating. Compared with the subjects with other psychiatric disorders, those with binge eating disorder reported more childhood obesity and more exposure to negative comments about shape, weight, and eating. Certain childhood traits and pronounced vulnerability to obesity distinguished the subjects with bulimia nervosa from those with binge eating disorder. Conclusions Binge eating disorder appears to be associated with exposure to risk factors for psychiatric disorder and for obesity. When compared with the wide range of risk factors for bulimia nervosa, the risk factors for binge eating disorder are weaker and more circumscribed. Premorbid perfectionism, negative self-evaluation, and vulnerability to obesity appear especially to characterize those in whom bulimia nervosa subsequently develops.

Journal ArticleDOI
TL;DR: The existence of neuroanatomical and neurobehavioral abnormalities in patients with first-episode schizophrenia indicates that the brain dysfunction occurred before clinical presentation, however, there is also evidence of progression, in which anatomical changes may affect some clinical and neuro behavioral features of the illness in some patients.
Abstract: Background: Cross-sectional neuroanatomical studies have reported abnormalities in schizophrenia that relate to disease variables. Longitudinal neuroimaging investigations that integrate anatomical, clinical, and neurobehavioral measures may help clarify the pathogenesis of schizophrenia. Methods: Magnetic resonance brain imaging and neurobehavioral studies were conducted at baseline and after 30.63±12.92 months (mean±SD) in 40 patients with schizophrenia (23 men and 17 women) and 17 healthy controls (13 men and 4 women). The schizophrenia group included 20 first-episode and 20 previously treated subjects. Volumes of whole-brain, cerebrospinal fluid, and frontal and temporal lobes were measured. The severity of negative and positive symptoms was assessed, medications were monitored, and neurobehavioral functioning in 8 domains was evaluated. Results: Both first-episode and previously treated patients had smaller brains and frontal and temporal lobes than controls at intake. Longitudinally, reduction in frontal lobe volume was found only in patients, whereas temporal lobe reduction was also seen in controls. The association between volume reduction and symptom changes differed between patient groups, but volume reduction was associated with decline in some neurobehavioral functions in both groups. Exploratory analysis suggested that neuroleptic dose is correlated with changes in all 3 domains. Conclusions: The existence of neuroanatomical and neurobehavioral abnormalities in patients with firstepisode schizophrenia indicates that the brain dysfunction occurred before clinical presentation. However, there is also evidence of progression, in which anatomical changes may affect some clinical and neurobehavioral features of the illness in some patients. Arch Gen Psychiatry. 1998;55:145-152

Journal ArticleDOI
TL;DR: Distinct cytometric abnormalities support the hypothesis that neuronal degeneration in the prefrontal cortex is not a prominent feature of the neuropathological changes in schizophrenia, although an ongoing process in Huntington disease.
Abstract: Background: The cortex of patients with schizophrenia exhibits a deficit in neuropil, but the nature and extent of cellular abnormalities remain unclear. To gain further insight into this abnormality, neuronal and glial somal size were analyzed in postmortem brains from 9 patients with schizophrenia, 10 normal (control) patients, and 7 patients with Huntington disease, the latter representing a known neurodegenerative disorder. Methods: A 3-dimensional image analyzer was used to measure the perimeters of 10 722 neuronal and 19 913 glial profiles in Brodmann areas 9 and 17. Neurons and glia were classified by size and layer to assess specific vulnerabilities with respect to cortical architecture and circuitry. Results: The schizophrenic prefrontal cortex was characterized by a downward shift in neuronal sizes accompanied by 70% to 140% per layer increases in the density of small neurons. In layer III only, a significant reduction in mean neuronal size was associated with a significant decrease in the density of very large neurons in sublayer IIIc. Neither neuronal size in occipital area 17 nor glial size in prefrontal or occipital cortexes were reduced. In cortex with Huntington disease, neuronal degeneration was evidenced by concurrence of reduced neuronal size, decreased density of large neurons, and dramatic elevation in density of large glia. Conclusions: Distinct cytometric abnormalities support the hypothesis that neuronal degeneration in the prefrontal cortex is not a prominent feature of the neuropathological changes in schizophrenia, although an ongoing process in Huntington disease. Rather, schizophrenia appears to involve more subtle abnormalities, with the largest corticocortical projection neurons of layer IIIc expressing the greatest somal reduction. Arch Gen Psychiatry. 1998;55:215-224

Journal ArticleDOI
TL;DR: Results of the acute treatment phase of a 2-site study comparing cognitive behavioral group therapy (CBGT) and treatment with the monoamine oxidase inhibitor phenelzine sulfate for social phobia suggest that these treatments can be efficacious at facilities with differing theoretical allegiances.
Abstract: Background This article presents results of the acute treatment phase of a 2-site study comparing cognitive behavioral group therapy (CBGT) and treatment with the monoamine oxidase inhibitor phenelzine sulfate for social phobia. Methods One hundred thirty-three patients from 2 sites received 12 weeks of CBGT, phenelzine therapy, pill placebo administration, or educational-supportive group therapy (an attention-placebo treatment of equal credibility to CBGT). The "allegiance effect," ie, the tendency for treatments to seem most efficacious in settings of similar theoretical orientation and less efficacious in theoretically divergent settings, was also examined by comparing responses to the treatment conditions at both sites: 1 known for pharmacological treatment of anxiety disorders and the other for cognitive behavioral treatment. Results After 12 weeks, phenelzine therapy and CBGT led to superior response rates and greater change on dimensional measures than did either control condition. However, response to phenelzine therapy was more evident after 6 weeks, and phenelzine therapy was also superior to CBGT after 12 weeks on some measures. There were few differences between sites, suggesting that these treatments can be efficacious at facilities with differing theoretical allegiances. Conclusions After 12 weeks, both phenelzine therapy and CBGT were associated with marked positive response. Although phenelzine therapy was superior to CBGT on some measures, both were more efficacious than the control conditions. More extended cognitive behavioral treatment and the combination of modalities may enhance treatment effect.

Journal ArticleDOI
TL;DR: In a population-based twin study of schizophrenia, heritability was estimated at 83%, with the remaining variance in liability attributed to environmental factors not shared in common among co-twins.
Abstract: Background The magnitude of heritability of schizophrenia remains controversial, due in part to limitations of estimates derived from index twin pairs exclusively. We applied structural equation modeling in a total population of twins to determine the significance and magnitudes of the genetic and environmental contributions to schizophrenia. Methods All monozygotic (1180 male and 1315 female pairs) and same-sex dizygotic (2765 male and 2613 female pairs) twins born from 1940 to 1957 in Finland were screened for nonorganic psychotic disorder diagnoses as recorded on an inpatient or outpatient basis or from an eligibility review for a disability pension. Results The lifetime prevalence of schizophrenia was 2.0%, with a marginally higher prevalence in men (2.2%) than women (1.8%). Model fitting indicated that 83% of the variance in liability was due to additive genetic factors, and the remaining 17% was due to unique environmental factors. Sex-limitation modeling revealed no evidence of sex-specific genetic effects and no sex difference in the magnitude of heritability. A multiple threshold model incorporating affective and other psychoses as a phenotype intermediate between schizophrenia and no diagnosis was rejected. Conclusions In a population-based twin study of schizophrenia, heritability was estimated at 83%, with the remaining variance in liability attributed to environmental factors not shared in common among co-twins. Despite the notable limitation of using diagnoses ascertained through treatment contacts, the heritability estimate in this study is almost identical to those reported in recent studies of index pairs using standardized applications of DSM-III or later criteria.

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TL;DR: Evidence indicates that both antidepressant pharmacotherapy and time-limited depression-targeted psychotherapies are efficacious when transferred from psychiatric to primary care settings.
Abstract: The Depression Guideline Panel of the Agency for Health Care Policy and Research in 1993 published recommendations for treating major depression in primary care practice that were often based on studies of tertiary care psychiatric patients. We reviewed reports of randomized controlled trials in primary care settings published between 1992 and 1998. This evidence indicates that both antidepressant pharmacotherapy and time-limited depression-targeted psychotherapies are efficacious when transferred from psychiatric to primary care settings. In most cases, the choice between these treatments should depend on patient preference. Studies to date suggest that improving treatment of depression in primary care requires properly organized treatment programs, regular patient follow-up, monitoring of treatment adherence, and a prominent role for the mental health specialist as educator, consultant, and clinician for the more severely ill. Future research should focus on how guidelines are best implemented in routine practice, since conventional dissemination strategies have little impact.

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TL;DR: It is suggested that the pathogenesis of tics involves an impaired modulation of neuronal activity in subcortical neural circuits in anatomically connected cortical regions believed to subserve attention-demanding tasks.
Abstract: Background: The inability to inhibit unwanted behaviors and impulses produces functional debility in a broad range of neuropsychiatric disorders. A potentially important model of impulse control is volitional tic suppression in Tourette syndrome. Methods Tic suppression was studied in 22 adult subjects with Tourette syndrome by using functional magnetic resonance imaging. Images acquired during periods of voluntary tic suppression were compared with images acquired when subjects allowed the spontaneous expression of their tics. The magnitudes of signal change in the images were then correlated with measures of the severity of tic symptoms. Conclusions Significant changes in signal intensity were seen in the basal ganglia and thalamus and in anatomically connected cortical regions believed to subserve attention-demanding tasks. The magnitudes of regional signal change in the basal ganglia and thalamus correlated inversely with the severity of tic symptoms. These findings suggest that the pathogenesis of tics involves an impaired modulation of neuronal activity in subcortical neural circuits.

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TL;DR: The results challenge the assumption that long-term drug treatment is the only tool to prevent relapse in patients with recurrent depression and suggest CBT offers a viable alternative for other patients.
Abstract: Background Cognitive behavioral treatment (CBT) of residual symptoms after successful pharmacotherapy yielded a substantially lower relapse rate than did clinical management in patients with primary major depressive disorders. The aim of this study was to test the effectiveness of this approach in patients with recurrent depression (≥3 episodes of depression). Methods Forty patients with recurrent major depression who had been successfully treated with antidepressant drugs were randomly assigned to either CBT of residual symptoms (supplemented by lifestyle modification and well-being therapy) or clinical management. In both groups, during the 20-week experiment, antidepressant drug administration was tapered and discontinued. Residual symptoms were measured with a modified version of the Paykel Clinical Interview for Depression. Two-year follow-up was undertaken, during which no antidepressant drugs were used unless a relapse ensued. Results The CBT group had a significantly lower level of residual symptoms after discontinuation of drug therapy compared with the clinical management group. At 2-year follow-up, CBT also resulted in a lower relapse rate (25%) than did clinical management (80%). This difference attained statistical significance by survival analysis. Conclusions These results challenge the assumption that long-term drug treatment is the only tool to prevent relapse in patients with recurrent depression. Although maintenance pharmacotherapy seems to be necessary in some patients, CBT offers a viable alternative for other patients. Amelioration of residual symptoms may reduce the risk of relapse in depressed patients by affecting the progression of residual symptoms to prodromes of relapse.

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TL;DR: Adherence to depression treatment guidelines with an antidepressant that is likely to have continuous use by patients reduces the probability of relapse or recurrence in a Medicaid population.
Abstract: Background Depression is associated with high rates of relapse and recurrence during a patient's lifetime. Current guidelines regarding treatment recommend 4 to 9 months of continuation antidepressant therapy following remission of acute symptoms to allow more complete resolution of the episode. In this article, we test whether adherence to these recommendations reduces the likelihood of relapse or recurrence in a Medicaid population. Methods We used a Medicaid database covering 1989 through 1994. The sample consists of the 4052 adult patients who filled an antidepressant prescription at the time of an initial diagnosis of depression. These patients were followed up for up to 2 years. Timing and counts of antidepressant prescription claims are used to construct a proxy measure for adherence to guidelines. Relapse or recurrence is defined by evidence of a new episode requiring antidepressant treatment, hospital admission for depression, electroconvulsive therapy, emergency department visit for mental health, or attempted suicide. We used survival analysis to predict relapse or recurrence for each patient and to examine the effect of following treatment guidelines on relapse and recurrence. Results Approximately one fourth of the patients had a relapse or recurrence during their follow-up period. Factors that affect relapse and recurrence include comorbidities, race, and guideline adherence. Those who continued therapy with their initial antidepressant were least likely to experience relapse or recurrence; those who discontinued their antidepressant early were most likely to experience relapse or recurrence. Conclusion Adherence to depression treatment guidelines with an antidepressant that is likely to have continuous use by patients reduces the probability of relapse or recurrence.

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TL;DR: In this paper, the neurocognitive performance of 25 euthymic bipolar patients (12 with and 13 without a history of alcohol dependence) were compared with 22 normal control subjects on a neuropsychological test battery assessing a range of cognitive domains.
Abstract: Background Few studies of the neurocognitive performance of patients with bipolar disorder have been performed while patients are in the euthymic state. Methods Twenty-five euthymic bipolar patients (12 with and 13 without a history of alcohol dependence) were compared with 22 normal control subjects on a neuropsychological test battery assessing a range of cognitive domains. The relationship between subjects' neurocognitive performance and the course-of-illness variables (lifetime episodes and duration of mania, depression, or both), as well as current lithium level, was determined. Results The results indicated differences across the groups, with the bipolar patients with and without alcohol dependence performing more poorly than controls on tests of verbal memory. Furthermore, bipolar subjects with a history of alcohol dependence had additional decrements in executive (ie, frontal lobe) functions when compared with controls. For subjects in the bipolar group, lifetime months of mania and depression were negatively correlated with performance in verbal memory and several executive function measures. Conclusions Our findings support the presence of persistent neurocognitive difficulties in patients with long-standing bipolar disorder who are not in the psychiatrically acute state or who are suffering the effects of alcohol abuse and suggest that there may be an aggregate negative effect of lifetime duration of bipolar illness on memory and frontal or executive systems.

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TL;DR: Both lifetime and current panic-depression comorbidity are markers for more severe, persistent and disabling illness.
Abstract: Background The National Comorbidity Survey is a nationally representative survey of the prevalences and correlates of DSM-III-R disorders in the US household population. Methods Retrospective age-at-onset reports were used to study predictive relationships between lifetime panic and depression. Results Strong associations were found between the lifetime prevalences of panic and major depressive episodes (odds ratios: for panic attacks with depression, 6.2; for panic disorder with depression, 6.8). These associations were not significantly influenced by the inclusion or exclusion of respondents with mania. Temporally primary depression predicted a first onset of subsequent panic attacks but not of panic disorder. Temporally primary panic attacks, with or without panic disorder and whether or not the panic was persistent, predicted a first onset of subsequent major depression. The associations between panic attack and depression were attenuated in models that controlled for prior traumatic life experiences and histories of other DSM-III-R disorders. Conclusions Lifetime panic-depression comorbidity characterizes most community respondents with panic disorder and a substantial few of those with major depression. The absence of a dose-response relationship suggests that primary panic attack is a marker, rather than a causal risk factor, of subsequent depression. Primary depression, in comparison, appears to be a genuine risk factor for secondary panic attacks. That primary depression predicts panic attacks but not panic disorder suggests that secondary panic is a severity marker of depression rather than a comorbid condition. These results are far from definitive because they are based on retrospective reports, lay-administered diagnostic interviews, and only 1 survey. However, they raise important questions that could lead to a fundamental rethinking of panic-depression comorbidity if they are replicated in future epidemiological and clinical studies.

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TL;DR: Elevated heart rate shortly after trauma is associated with the later development of posttraumatic stress disorder (PTSD).
Abstract: Background Physiological arousal during traumatic events may trigger the neurobiological processes that lead to posttraumatic stress disorder (PTSD). This study prospectively examined the relationship between heart rate and blood pressure recorded immediately following a traumatic event and the subsequent development of PTSD. Methods Eighty-six trauma survivors who presented at the emergency department of a general hospital were followed up for 4 months. Heart rate and blood pressure were recorded on arrival at the emergency department. Heart rate, anxiety, depression, and PTSD symptoms were assessed 1 week, 1 month, and 4 months later. The clinician-administered PTSD scale defined PTSD status at 4 months. Results Twenty subjects (23%) met PTSD diagnostic criteria at the 4-month assessment (PTSD group), and 66 (77%) did not (non-PTSD group). Subjects who developed PTSD had higher heart rates at the emergency department (95.5±13.9 vs 83.3±10.9 beats per minute, t =4.4, P .001) and 1 week later (77.8±11.9 vs 72.0±9.5 beats per minute, t =2.25, P .03), but not after 1 and 4 months. The groups did not differ in initial blood pressure measurement. Repeated-measures analysis of variance (ANOVA) for heart rate showed a significant group effect ( P .02), time effect ( P .001), and group × time interaction ( P .001). The time effect and group × time interaction remained significant when adjusted for sex, age, trauma severity, immediate response, and dissociation during the traumatic event. Conclusion Elevated heart rate shortly after trauma is associated with the later development of PTSD.