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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present report describes the development of the Penn State Worry Questionnaire to measure the trait of worry. The 16-item instrument emerged from factor analysis of a large number of items and was found to possess high internal consistency and good test-retest reliability. The questionnaire correlates predictably with several psychological measures reasonably related to worry, and does not correlate with other measures more remote to the construct. Responses to the questionnaire are not influenced by social desirability. The measure was found to significantly discriminate college samples (a) who met all, some, or none of the DSM-III-R diagnostic criteria for generalized anxiety disorder and (b) who met criteria for GAD vs posttraumatic stress disorder. Among 34 GAD-diagnosed clinical subjects, the worry questionnaire was found not to correlate with other measures of anxiety or depression, indicating that it is tapping an independent construct with severely anxious individuals, and coping desensitization plus cognitive therapy was found to produce significantly greater reductions in the measure than did a nondirective therapy condition.
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PMID:Development and validation of the Penn State Worry Questionnaire. 207 86

The blind test-retest reliability of lifetime prevalence and age of onset of psychiatric diagnoses, based on the SADS-L interview and RDC over a three-to-five year period, was examined in 143 probands and their relatives. Reliability of lifetime prevalence of major depression was excellent; reliability of antisocial personality, panic disorder, drug abuse, GAD, depressive personality, and alcoholism was good; reliability of obsessive-compulsive disorder and phobia was acceptable but lower. The reliability of hyperthymia or cyclothymia was not acceptable. Reliability for major depression did not vary substantially by age or sex of the informant, but recall of major depression was significantly higher in the probands than in their relatives. The test-retest reliability for the age of onset of major depression and panic disorder was excellent, and for phobia, GAD and alcoholism, was acceptable. Both probands and relatives recalled the age of onset of their depression fairly accurately. However, there was a reduction in agreement over time. Recall after 3-4 yr was better than 5-6 yr. There was a tendency for older respondents to systematically increase the age of onset of their depression across the two interviews, although the increase was only a few years. Recall of age of onset did not differ significantly by sex of respondent or whether the respondent was a proband or relative. These findings are discussed in light of several available studies of reliability of lifetime prevalence of psychiatric diagnoses.
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PMID:Lifetime prevalence and age of onset of psychiatric disorders: recall 4 years later. 326 42

Generalized anxiety disorder is a relatively new clinical entity and current understanding of this syndrome lacks a solid research base. However, useful generalizations can be derived from earlier studies of anxiety neurosis and other previously defined anxiety syndromes. Most persons with GAD are seen by primary care physicians, but recognizing these patients may be difficult. In the primary care setting they often present with physical complaints suggesting a specific organ system disease. Depression and substance abuse may be presenting problems in patients with primary GAD. Primary care physicians are usually able to provide appropriate care for generalized anxiety disorder patients. By keeping in mind the cognitive, behavioral, affective, and physiologic aspects of the syndrome, they can appropriately address the specific therapeutic needs of individual patients. The nature of the doctor-patient relationship in primary care favors the development of therapeutic trust that is important for effective management of GAD. Drug therapy is a useful adjunct in the treatment of many patients with GAD. However, the use of drugs as the sole therapeutic modality is seldom appropriate.
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PMID:Generalized anxiety disorder. 332 27

Amitryptyline (10 mg/kg), desipramine (5 mg/kg), citalopram (10 mg/kg) and viloxazine (10 mg/kg) were administered to rats either acutely (decapitation 1 hr after i.p. injection) or subacutely (by subcutaneous minipump implantation for 18 days followed by decapitation 24 hr after removal). After acute administration there was not any consistent alteration in GABA levels, GAD activity, 3H GABA "A" or 3H-GABA "B" receptor binding or 3H-nipecotic acid binding to the recognition site for GABA uptake in the frontal cortex or hippocampus. Upon subacute antidepressant drug infusion, GABA levels, GAD activity and 3H-GABA-"A" binding showed only scattered differences in drug treated animals as compared to saline treated rats. However, 3H-GABA "B" binding in the frontal cortex was consistently elevated after all drug treatments (in % of control: amitryptyline = 155%; desipramine = 151%; citalopram = 173%; viloxazine = 189%). Scatchard analysis showed that this was due to a Bmax increase without an effect in Kd. These findings were reproduced by subacute administration of pargyline, a MAO inhibitor. These data suggest that GABA "B" receptors may be involved in the mechanism of action of antidepressant drugs and provide a link between GABAergic and monoaminergic hypotheses of depression.
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PMID:Chronic antidepressants and GABA "B" receptors: a GABA hypothesis of antidepressant drug action. 609 15

A previous paper, Butler and Anastasiades (Behaviour Research and Therapy 26, 531-534, 1988) presented evidence for three reliable predictors of response to Anxiety Management in patients with generalised anxiety disorder. It was argued there that these reflected severity of anxiety, demoralisation and depression. A second study (Butler, Fennell, Robson & Gelder, Journal of Consulting and Clinical Psychology, 59, 167-175, 1991) has compared two treatments for GAD: Behaviour Therapy and Cognitive Behaviour Therapy. Data from this study is used here to answer two questions: (i) do the same three variables predict outcome in the second study? The answer to this question is 'no'; and (ii) which variables contribute to prediction of outcome when these two treatments are compared? Information presented here suggests that this depends partly on the nature of the treatment given. Outcome after behaviour therapy is predicted by initial levels of anxiety only, but the gains made are also relatively modest. Outcome after cognitive behaviour therapy is predicted by the degree to which ambiguous (external) information is interpreted as threatening. Thus a cognitive variable contributes reliably to the prediction of outcome after a cognitive treatment, but does not predict in the same way to outcome after a behavioural treatment.
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PMID:Predicting outcome after treatment for generalised anxiety disorder. 844 48

GAD generally is a fairly prevalent disorder occurring at a rate (even in its "pure" form) that equals or exceeds the other anxiety disorders such as panic disorder and social phobia. GAD tends to have an early age of onset and tends to exhibit a high degree of chronicity that frequently is complicated by comorbidity with other anxiety disorders as well as by depression and other Axis I and II disorders. The pharmacologic treatment of GAD should be conceptualized from the first day of treatment in terms of the long-term nature of the illness, in much the same way that treatment of affective disorders is now conceptualized. And yet an enormous amount of research remains to be done, as we know very little from controlled studies about how to optimize maintenance treatment of this relatively neglected disorder.
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PMID:Generalized anxiety disorder. Longitudinal course and pharmacologic treatment. 874 84

Using outpatients with anxiety and mood disorders (N = 350), the authors tested several models of the structural relationships of dimensions of key features of selected emotional disorders and dimensions of the tripartite model of anxiety and depression. Results supported the discriminant validity of the 5 symptom domains examined (mood disorders: generalized anxiety disorder, GAD; panic disorder; obsessive-compulsive disorder; social phobia). Of various structural models evaluated, the best fitting involved a structure consistent with the tripartite model (e.g., the higher order factors, negative affect and positive affect, influenced emotional disorder factors in the expected manner). The latent factor, GAD, influenced the latent factor, autonomic arousal, in a direction consistent with recent laboratory findings (autonomic suppression). Findings are discussed in the context of the growing literature on higher order trait dimensions (e.g., negative affect) that may be of considerable importance to the understanding of the pathogenesis, course, and co-occurrence of emotional disorders.
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PMID:Structural relationships among dimensions of the DSM-IV anxiety and mood disorders and dimensions of negative affect, positive affect, and autonomic arousal. 960 48

The prevalence and clinical impact of anxiety disorder comorbidity in major depression were studied in 255 depressed adult outpatients consecutively enrolled in our Depression Research Program. Comorbid anxiety disorder diagnoses were present in 50.6% of these patients and included social phobia (27.0%), simple phobia (16.9%), panic disorder (14.5%), generalized anxiety disorder ([GAD] 10.6%), obsessive-compulsive disorder ([OCD] 6.3%), and agoraphobia (5.5%). While both social phobia and generalized anxiety preceded the first episode of major depression in 65% and 63% of cases, respectively, panic disorder (21.6%) and agoraphobia (14.3%) were much less likely to precede the first episode of major depression than to emerge subsequently. Although comorbid groups were not distinguished by depression, anxiety, hostility, or somatic symptom scores at the time of study presentation, patients with comorbid anxiety disorders tended to be younger during the index episode and to have an earlier onset of the major depressive disorder (MDD) than patients with major depression alone. Our results support the distinction between anxiety symptoms secondary to depression and anxiety disorders comorbid with major depression, and provide further evidence for different temporal relationships with major depression among the several comorbid anxiety disorders.
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PMID:Anxiety disorders in major depression. 1074 86

This report examines clinical features of generalized anxiety disorder in adolescents and young adults with mild mental retardation (MR), compared with children and adolescents with normal IQ. Frequency of symptoms, comorbidity, agreement between reports of subjects and parents, correlation between IQ and severity of disorder, and comparison between frequency of symptoms in the experimental and control groups are described. Twenty-two subjects with MR (12 males and 10 females aged 11-25 years; mean age = 16.3), 30 children (19 males and 11 females aged 7-11.11; mean age = 10), and 30 adolescents (18 males and 12 females aged 12.1-18; mean age = 15.2) participated in the study. All the subjects were comprehensively diagnosed with diagnostic interviews (K-SADS or DICA-R). According to our data, generalized anxiety disorder can be diagnosed in adolescents with mild MR, with high agreement between self-reports and parent reports. Phenomenology of GAD in mildly developmentally delayed persons grossly paralleled that of normal IQ people, except for brooding, somatic complaints, and sleep disorders. Number and severity of symptoms did not correlate with Full Scale and Verbal IQs. High rates of comorbidity with depression were evident both in normal IQ and in developmentally delayed subjects.
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PMID:Generalized anxiety disorder in adolescents and young adults with mild mental retardation. 1085 60

Hypochondriasis is a heterogeneous disorder. This was well demonstrated in the study by Kellner et al, which showed that patients with high levels of disease fear tended to be more anxious or phobic, whereas patients with high levels of disease conviction tended to have more and more severe somatic symptoms. Little comorbidity exists to support the statement that hypochondriasis is an obsessive-compulsive spectrum disorder. Although patients exist whose hypochondriac concerns are identical in quality to the intrusive thoughts of patients with OCD, as a group, patients with hypochondriasis do not share a comorbidity profile comparable with that of patients with OCD. The data support a closer relationship between hypochondriasis and somatization disorder than between hypochondriasis and OCD. The family history data is limited by the lack of adequate studies. Using comparable methods of the family history approach, Black's study reported a higher frequency of GAD but not OCD among the relatives of OCD patients--a finding similar to what Noyes found among the relatives of hypochondriac patients; however, using the direct interview method, somatization disorder was the only statistically more common disorder, among relatives of female hypochondriac patients. Therefore, although the parallel in overlap with GAD is suggestive of a commonality between OCD, GAD, and hypochondriasis, the finding of a greater frequency of somatization disorder leans against the hypothesis that hypochondriasis is best considered an OCD spectrum disorder. The pharmacologic treatment data are the one type of biologic evidence that supports a bridge to OCD. The pharmacologic studies suggest that for patients with general hypochondriasis, TCAs are not effective and that higher dosages and longer trials of the SRIs are needed. These pharmacologic observations are comparable with the ones made for patients with OCD but dissimilar to the observations made for depression. The benefit of imipramine among patients with illness phobia must be assessed in placebo-controlled trials among illness phobics and among hypochondriacs. Even more valuable would be a direct comparison of a TCA (e.g., imipramine or desipramine) and a selective SRI (e.g., fluoxetine) to determine whether the response to selective SRIs is greater. Although the pharmacologic data are compelling in supporting the hypothesis that hypochondriasis is an obsessive-compulsive spectrum disorder, the comorbidity data are equally compelling in dispelling that hypothesis. Perhaps future studies clarify the subtypes of hypochondriasis, be they "phobic, obsessive, and depressive," "chronic and episodic," "early onset versus late onset" or some other as yet undetermined subtype. Such clarification may be aided by better instruments to assess the obsessive-compulsive and hypochondria spectrums within individuals and families and by neuropsychological or pharmacologic challenge and neuroimaging studies.
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PMID:Hypochondriasis and its relationship to obsessive-compulsive disorder. 1098 30


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