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

The novel anxiolytic agent buspirone has been shown to be effective in generalized anxiety disorder, but its utility in phobic disorders is less clear. We examined its efficacy in social phobia in a 12-week open trial. Twenty-one patients who met DSM-III-R criteria for social phobia and who did not respond to 1 week of single-blind placebo were treated with buspirone, and 17 completed a minimum of 2 weeks of treatment. Twelve of these 17 patients met criteria for the generalized subtype of social phobia. At week 12, 8 (47%) of the 17 patients were rated much to very much improved in social phobia symptoms on the Clinical Global Impression Scale. Of the 12 patients who were able to tolerate a dose of 45 mg/day or more, 9 (67%) were at least much improved. Significant improvement was noted on measures of social anxiety and avoidance of social situations. Ratings of generalized anxiety and depression, which were low at baseline, did not change significantly during treatment. The results suggest that buspirone may have modest efficacy in the treatment of social phobia, but confirmation in a placebo-controlled trial is required.
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PMID:Buspirone in social phobia. 837 12

Beta-adrenergic receptor kinetics were measured in leukocytes from 17 drug-free, nondepressed patients with social phobia (generalized type) and 17 gender-matched and age-matched healthy controls. Binding was characterized using the highly specific beta-adrenergic ligand [125I]pindolol (125IPIN). Contrary to some studies in panic disorder and many studies in depression, no significant difference was found in Bmax or Kd values between social phobic patients and controls. Neither severity of social phobic symptoms nor the severity of certain symptoms of beta-adrenergic activation (i.e., tachycardia, tremor, blushing) influenced Bmax or Kd. To the extent that these peripheral indices can be considered reflective of central processes, these findings suggest that a simple defect in beta-adrenoceptor number of affinity is unlikely to explain the pathophysiology of generalized social phobia.
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PMID:Lymphocyte beta-adrenoceptors in social phobia. 839 92

Although theoretical explanations for comorbidity in panic disorder (PD) abound in the literature, the complex clinical challenges of these patients have been neglected, especially where panic, obsessive-compulsive and 'soft' bipolar (e.g., hypomanic, cyclothymic and hyperthymic) conditions might co-exist. The aim of the present study has been to systematically explore the spectrum of intra-episodic and longitudinal comorbidity of 140 DSM-III-R PD patients--67.1% of whom concomitantly met the criteria for Agoraphobia--and who were consecutively admitted to the ambulatory service of the Psychiatric Clinic of the University of Pisa over a 2-year period. Comorbidity with strictly defined anxiety disorders--i.e., not explained as mere symptomatic extensions of PD--was relatively uncommon, and included Simple Phobia (10.7%), Social Phobia (6.4%), Generalized Anxiety Disorder (3.6%), and Obsessive-Compulsive Disorder (4.2%). Comorbidity with Major Depression--strictly limited to the melancholic subtype--occurred in 22.9%. Comorbidity with Bipolar Disorders included 2.1% with mania, 5% with hypomania, as well as 6.4% with cyclothymia, for a total of 13.5%; an additional 34.3% of PD patients met the criteria for hyperthymic temperament. We submit that such comorbid patterns are at the root of unwieldy clinical constructs like 'atypical depression' and 'borderline personality'. The relationship of panic disorder to other anxious-phobic and depressive states has been known for some time. Our data extend this relationship to soft bipolar disorders. Studies from other centers are needed to verify that the proposed new link is not merely due to referral bias to a tertiary university setting.
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PMID:Affective comorbidity in panic disorder: is there a bipolar connection? 840 78

Neuromuscular block can cause anxiety. These known experimental results lead to the expectation of conditioned phobic reactions in myasthenia gravis. A sample of 240 patients with the disease do not show the theoretically expected results in the Fear-Survey-Schedule. But interindividual variation of anxiety corresponds to some clinical parameters, relevant for the disease. Patients with facial muscular symptoms have higher values on social phobia but no higher scores on a depression-scale. Opposite to the facial-feedback theory, this result supports the hypothesis, that intersubjective feedback is more significant to the development of the emotional reaction than proprioceptive (facial) feedback. Social anxiety also covariates with defensive coping-strategies. Implications for supportive psycho(behaviour)therapy are discussed.
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PMID:[Situational anxiety in myasthenia gravis]. 846 68

Hirsutism is recognized to cause profound distress in affected women, due to cosmetic and psychosexual implications. It was evaluated in the present study by methods found to be valid and reliable in psychosomatic research. Fifty women with hirsutism belonging to the spectrum of disorders from idiopathic hirsutism to polycystic ovary syndrome, after complete medical work-up, underwent the same psychometric evaluation as 50 healthy non-hirsute women, matched for sociodemographic variables. Hirsute women had a Ferriman and Gallwey score ranging from 8 to 19. Psychometric evaluation for quality of life was carried out by the following methods: (a) Kellner's Brief Problem List, a 12 item self-rating list of psychosocial problems; (b) Kellner's Symptom Rating Test (SRT), a 46 item self-rating scale that yields a total score of distress as well as six subscales (anxiety, depression, somatic symptoms, anger-hostility, cognitive and psychotic symptoms); and (c) Marks' Social Situations Questionnaire (SSQ), a 30 item self-rating scale concerned with social phobia. Patients with hirsutism displayed significantly higher social fears at the SSQ than controls (P < 0.01). They also showed more anxiety (P < 0.01) and psychotic symptoms (P < 0.01) at the SRT, whereas there were no significant differences in depression, somatization, anger-hostility and cognitive symptoms. These results suggest that the complex management of hirsute women, in addition to pharmacological and/or cosmetic measures, may require specific psychotherapy.
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PMID:Quality of life of hirsute women. 849 31

Outcome of anxiety disorder treatment with psychotherapy and medication is generally as good as or better than that of other psychiatric illnesses. Nevertheless, refractory cases occur. The first step in approaching the treatment-resistant patient with an anxiety disorder is to be certain that the treatment has been adequate. Failure to provide an adequate dose of medication for adequate periods of time may be the most common cause of "treatment resistance." The second step is to reconsider the diagnosis and/or determine if new diagnoses have emerged since the original consultation. Depression and substance abuse are especially likely to complicate anxiety disorders. Several studies have shown that concomitant personality disorders (axis II) increase the occurrence of resistance to standard treatment and must be addressed through psychotherapy. Last, a variety of possible underlying medical conditions, including thyroid disorder, arrhythmia, and complex partial seizure, should be considered. Then, the clinician should consider a variety of pharmacologic approaches that are specific to each anxiety disorder. Panic disorder patients who are refractory to imipramine frequently respond to high-potency benzodiazepines, monoamine oxidase (MAO) inhibitors, serotonin reuptake inhibitors, or various combinations. Generalized anxiety disorder, if unresponsive to benzodiazepines, may respond to buspirone or a tricyclic antidepressant. Patients with obsessive compulsive disorder who have failed to respond to clomipramine or fluoxetine and other serotonin reuptake blockers may benefit from augmentation strategies using combination therapies including buspirone, fenfluramine, and neuroleptics. Social phobia refractory to beta-blockers and MAO inhibitors may benefit from buspirone, fenfluramine, and neuroleptics. Social phobia refractory to beta-blockers and MAO inhibitors may benefit from buspirone, fluoxetine, or alprazolam.
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PMID:Therapeutic strategies for the patient with treatment-resistant anxiety. 850 58

Sixty-seven subjects, including normal volunteers and patients with obsessive-compulsive disorder, social phobia, and borderline personality disorder, received ratings of depersonalization after double-blind, placebo-controlled challenges with the partial serotonin agonist meta-chlorophenylpiperazine (m-CPP). Challenge with m-CPP induced depersonalization significantly more than did placebo. Subjects who became depersonalized did not differ in age, sex, or diagnosis from those who did not experience depersonalization. There was a significant correlation between the induction of depersonalization and increase in panic, but not nervousness, anxiety, sadness, depression, or drowsiness. This report suggests that serotonergic dysregulation may in part underlie depersonalization.
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PMID:Induction of depersonalization by the serotonin agonist meta-chlorophenylpiperazine. 857 Jul 68

Seventy-seven patients with a primary diagnosis of social phobia (DSM-III-R) were randomized to treatment with the reversible and selective monoamine oxidase type A inhibitor brofaromine (n = 37) or placebo (n = 40) for 12 weeks in a double-blind trial. A fixed dose of 150 mg/day or a matching placebo was given after a 2-week dose titration phase. Patients with additional diagnoses of simple phobia, generalized anxiety disorder, dysthymia or major depressive disorder currently in remission were accepted. Patients with other Axis I mental disorders were excluded. In the brofaromine group, 78% of the patients scored much or very much improved on the Clinical Global Impression scale compared with 23% in the placebo group. The anxiety and avoidance scores on the Liebowitz Social Anxiety Scale (LSAS) were significantly reduced in favor of brofaromine. The clinical effects were not significantly correlated with the plasma concentration of brofaromine. After 12 weeks the brofaromine group scored significantly lower than the placebo group on a core depression part of the Montgomery-Asberg Depression Rating Scale. After 12 weeks of treatment the brofaromine group had significantly higher total scores on the LSAS than an age- and gender-matched group of healthy controls. The brofaromine group improved further during 9-month follow-up treatment period, whereas 60% of the placebo responders who continued long-term treatment relapsed. The most common side effects in the brofaromine group were sleep disturbances, dry mouth and nausea.
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PMID:Social phobia: the clinical efficacy and tolerability of the monoamine oxidase -A and serotonin uptake inhibitor brofaromine. A double-blind placebo-controlled study. 861 39

Children referred for growth hormone (GH) treatment have increased school achievement problems, lack appropriate social skills and show several forms of behavior problems. A multicenter study in the United States has revealed that many GH-impaired children exhibit a cluster of behavioral symptoms involving disorders of mood and attention. Anxiety, depression, somatic complaints and attention deficits have been identified. These symptoms decline in frequency over a period of 3 years, beginning shortly after GH replacement therapy is started. Many of the patients who have received GH and had good growth responses show lower than average quality of life in young adulthood after treatment is completed. GH-deficient adults placed on GH therapy report improvement in psychological well-being and health status, suggesting that GH might have a central neuroendocrine action. Among a group of adults who were GH deficient as children, we find a high incidence of social phobia, a psychiatric disorder linked to GH secretion and usually accompanied by poor life quality. An ongoing study of non-GH-deficient short individuals suggests that short stature is not the cause of this outcome. We conclude that the origins of psychiatric comorbidities, such as social phobia and depression, in GH deficient adults are likely to be neuroendocrine as well as psychosocial.
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PMID:Links between growth hormone deficiency, adaptation and social phobia. 874 15

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


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