The development ofa 2 l-item self-report inventory for measuring the severity of anxiety in psychiatric populations is described. The initial item pool of 86 items was drawn from three preexisting scales: the Anxiety Checklist, the Physician's Desk Reference Checklist, and the Situational Anxiety Checklist. A series of analyses was used to reduce the item pool. The resulting Beck Anxiety Inventory (BAI) is a 21-item scale that showed high internal consistency (a = .92) and test-retest reliability over 1 week, r(81) = .75. The BAI discriminated anxious diagnostic groups (panic disorder, generalized anxiety disorder, etc.) from nonanxious diagnostic groups (major depression, dysthymic disorder, etc). In addition, the BAI was moderately correlated with the revised Hamilton Anxiety Rating Scale, r(150) = .51, and was only mildly correlated with the revised Hamilton Depression Rating Scale, r(l 53) = .25.

Describes the rationale, development, and validation of the Scale for Suicide Ideation, a 19-item clinical research instrument designed to quantify and assess suicidal intention. In a sample with 90 hospitalized Ss, the scale was found to have high internal consistency and moderately high correlations with clinical ratings of suicidal risk and self-administered measures of self-harm. Furthermore, it was sensitive to changes in levels of depression and hopelessness (Beck Depression Inventory and Hopelessness Scale, respectively) over time. Its construct validity was supported by 2 studies by different investigators testing the relationship between hopelessness, depression, and suicidal ideation and by a study demonstrating a significant relationship between high level of suicidal ideation and "dichotomous" attitudes about life and related concepts on a semantic differential test. Factor analysis yielded 3 meaningful factors: Active Suicidal Desire, Specific Plans for Suicide, and Passive Suicidal Desire. (29 ref)

This review summarizes the current meta-analysis literature on treatment outcomes of CBT for a wide range of psychiatric disorders. A search of the literature resulted in a total of 16 methodologically rigorous meta-analyses. Our review focuses on effect sizes that contrast outcomes for CBT with outcomes for various control groups for each disorder, which provides an overview of the effectiveness of cognitive therapy as quantified by meta-analysis. Large effect sizes were found for CBT for unipolar depression, generalized anxiety disorder, panic disorder with or without agoraphobia, social phobia, posttraumatic stress disorder, and childhood depressive and anxiety disorders. Effect sizes for CBT of marital distress, anger, childhood somatic disorders, and chronic pain were in the moderate range. CBT was somewhat superior to antidepressants in the treatment of adult depression. CBT was equally effective as behavior therapy in the treatment of adult depression and obsessive-compulsive disorder. Large uncontrolled effect sizes were found for bulimia nervosa and schizophrenia. The 16 meta-analyses we reviewed support the efficacy of CBT for many disorders. While limitations of the meta-analytic approach need to be considered in interpreting the results of this review, our findings are consistent with other review methodologies that also provide support for the efficacy CBT. D 2005 Elsevier Ltd. All rights reserved.Cognitive-behavioral therapy is one of the most extensively researched forms of psychotherapy. Over 120 controlled clinical trials were added to the literature in the eight years between 1986(Hollon & Beck, 1994 and this proliferation has continued (Dobson, 2001). There are now over 325 published outcome studies on cognitive-behavioral interventions. This growth is due in part to the ongoing adaptation of CBT for an increasingly wider range of disorders and problems (Beck, 1997;Salkovskis, 1996). Yet, many questions remain regarding the overall effectiveness of CBT, its differential effectiveness by disorder, the nature of the control groups by which its effectiveness has been established, and the extent to which its effects persist following the cessation of treatment. In this paper we review evidence from meta-analyses that address these questions. Our approach is unique in that we systematically summarize findings across high-quality meta-analyses for 16 different disorders. We focus on direct comparisons of CBT to alternative treatments wherever possible.A review of meta-analyses on CBT outcomes is particularly relevant to the ongoing debate about the comparative efficacy of different treatments (Rounsaville & Carroll, 2002). For instance, a recent review of meta-analyses and 0272-7358/$ -see front matter D

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Although the cognitive model of depression has evolved appreciably since its first formulation over 40 years ago, the potential interaction of genetic, neurochemical, and cognitive factors has only recently been demonstrated. Combining findings from behavioral genetics and cognitive neuroscience with the accumulated research on the cognitive model opens new opportunities for integrated research. Drawing on advances in cognitive, personality, and social psychology as well as clinical observations, expansions of the original cognitive model have incorporated in successive stages automatic thoughts, cognitive distortions, dysfunctional beliefs, and information-processing biases. The developmental model identified early traumatic experiences and the formation of dysfunctional beliefs as predisposing events and congruent stressors in later life as precipitating factors. It is now possible to sketch out possible genetic and neurochemical pathways that interact with or are parallel to cognitive variables. A hypersensitive amygdala is associated with both a genetic polymorphism and a pattern of negative cognitive biases and dysfunctional beliefs, all of which constitute risk factors for depression. Further, the combination of a hyperactive amygdala and hypoactive prefrontal regions is associated with diminished cognitive appraisal and the occurrence of depression. Genetic polymorphisms also are involved in the overreaction to the stress and the hypercortisolemia in the development of depression--probably mediated by cognitive distortions. I suggest that comprehensive study of the psychological as well as biological correlates of depression can provide a new understanding of this debilitating disorder.

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The relation of hopelessness to levels of depression and suicidal intent was explored both psychometrically and clinically. The results of an investigation of 384 suicide attempters support previous reports that hopelessness is the key variable linking depression to suicidal behavior. This finding has direct implications for the therapy of suicidal individuals. By focusing on reducing the sources of a patient's hopelessness, the professional may be able to alleviate suicidal crises more effectively than in the past.

We present a linear rank preserving model (RPM) approach for analyzing mediation of a randomized baseline intervention's effect on a univariate follow-up outcome. Unlike standard mediation analyses, our approach does not assume that the mediating factor is also randomly assigned to individuals in addition to the randomized baseline intervention (i.e., sequential ignorability), but does make several structural interaction assumptions that currently are untestable. The G-estimation procedure for the proposed RPM represents an extension of the work on direct effects of randomized intervention effects for survival outcomes by Robins and Greenland (1994, Journal of the American Statistical Association 89, 737-749) and on intervention non-adherence by Ten Have et al. (2004, Journal of the American Statistical Association 99, 8-16). Simulations show good estimation and confidence interval performance by the proposed RPM approach under unmeasured confounding relative to the standard mediation approach, but poor performance under departures from the structural interaction assumptions. The trade-off between these assumptions is evaluated in the context of two suicide/depression intervention studies.