Social anxiety disorder, also known as social phobia, is one of the most prevalent anxiety disorders, affecting 7-13% of subjects in the community at some time in their lives. Despite being eminently treatable, it remains largely under-recognised and, therefore, undertreated. The disorder is characterized by a fear of scrutiny by others, with sufferers experiencing excessive anxiety in social and performance situations. This excessive anxiety usually leads to avoidance behaviour that can severely affect normal daily living. With onset commonly occurring during childhood or adolescence, social anxiety disorder may disrupt normal patterns of development of social and personal relationships, often having a long-term impact on emotional stability in social or working life. If left untreated, the course of social anxiety disorder is frequently complicated with comorbid conditions, particularly major depression or substance abuse. This review assesses the size of the clinical problem by evaluating current and lifetime prevalence estimates, age of onset, risk factors and evolution of the clinical course; thereby providing the rationale for early recognition and prompt treatment.

The objective was to examine duloxetine 60–120mg/day treatment for relapse prevention in adults with generalized anxiety disorder (GAD). Adult patients (N=887; mean age=43.3 years; 61.0% female) with DSM-IV-TR-defined GAD diagnosis were treated with duloxetine for 26 weeks. Patients who completed open-label phase and were treatment responders (≥50% reduction in Hamilton Anxiety Rating Scale total score to ≤11 and “much”/“very much improved” ratings for the last 2 visits of open-label phase) were randomly assigned to receive duloxetine or placebo for a 26-week double-blind continuation phase. Relapse was defined as ≥2-point increase in illness severity ratings or by discontinuation due to lack of efficacy. During the double-blind phase, placebo-treated patients (N=201) relapsed more frequently (41.8%) than duloxetine-treated patients (13.7%, N=204, P≤0.001) and worsened on each outcome measure (P≤0.001, all comparisons). Duloxetine 60–120 mg/day treatment was efficacious and reduced risk of relapse in patients with GAD.

Der Beitrag untersucht auf der Grundlage neuer primärärztlicher Befunde die Versorgungsqualität bei der hinsichtlich Chronizität und Arbeitsausfall schwerwiegendsten Angsterkrankung, der Generalisierten Angststörung. Neben einer knappen Einführung in das Störungsbild werden die an über 20 000 Patienten in 558 Hausarztpraxen gewonnenen Kernbefunde der GAD-P-Studie (Generalisierte Angst und Depression in der Primärärztlichen Versorgung) zusammengefasst und Ansatzpunkte zur Verbesserung der Versorgungsqualität dieses selten adäquat behandelten Störungsbildes diskutiert. Insbesondere wird auf die zentrale Bedeutung einer sichereren diagnostischen Erkennung als Voraussetzung für therapeutische Verbesserungen hingewiesen. In Ergänzung zur Verbesserung bestehender Weiterbildungsangebote wird auf Arzt- und Patientenebene der breitere Einsatz bestehender Screeningverfahren, die Nutzung krankheitsspezifischer Patientenratgeber, sowie eine breitere Öffentlichkeitsarbeit zur Information über dieses bislang vernachlässigte, häufig chronisch verlaufende Krankheitsbild empfohlen. / Based on new empirical findings in a large-scale primary care study, the quality of care for the most chronic and debilitating anxiety problem, generalised anxiety disorder, is examined. Following a brief introduction of this disorder, the core findings of the GAD-P study (generalised anxiety and depression in primary care) with more than 20,000 patients of 558 family doctor practices are summarised and measures to improve the quality of care of patients with generalised anxiety disorder, a disorder which is rarely adequately treated, are discussed. This paper particularly emphasises the standard use of time-efficient diagnostic screening instruments, because improved recognition and diagnosis is the prerequisite for appropriate treatment. Further the role of the media to increase awareness of this disorder as well as patient education materials to improve compliance and to enhance treatment outcome effects are highlighted.

We examined parental psychopathology and family environment in subthreshold and DSM-IV threshold conditions of social anxiety disorder (SAD) in a representative cohort sample of 1,395 adolescents. Offspring and parental psychopathology was assessed using the DIAX/ M-CIDI; recalled parental rearing and family functioning via questionnaire. Diagnostic interviews in parents were supplemented by family history reports from offspring. The cumulative lifetime incidence was 23.07% for symptomatic SAD, and 18.38 and 7.41% for subthreshold and threshold SAD, respectively. The specific parent-tooffspring association for SAD occurred for threshold SAD only. For subthreshold and threshold SAD similar associations were found with other parental anxiety disorders, depression and substance use disorders. Parental rearing behaviour, but not family functioning, was associated with offspring threshold SAD, and although less strong and less consistent, also with subthreshold SAD. Results suggest a continued graded relationship between familial risk factors and offspring SAD. Parental psychopathology and negative parental styles may be used defining high-risk groups to assign individuals with already subthreshold conditions of SAD to early intervention programs.

Background. To examine the role of parental psychopathology and family environment for the risk of social anxiety disorder (SAD) in offspring from childhood to early adulthood, covering an observational period of 10 years. Method. A community sample of 1,395 adolescents (aged 14 to 17 years at baseline) was prospectively followed-up over the core high risk period for SAD onset. DSM-IV offspring and parental psychopathology was assessed using the Munich-Composite International Diagnostic Interview; direct diagnostic interviews in parents were supplemented by family history reports from offspring. Parental rearing was assessed by the Questionnaire of Recalled Rearing Behavior in offspring, family functioning by the McMaster Family Assessment Device in parents. Results. Parental SAD was associated with the offspring’s risk to develop SAD (OR = 3.3, 95%CI: 1.4-8.0). Additionally, other parental anxiety disorders (OR = 2.9, 95%CI: 1.4-6.1), depression (OR = 2.6, 95%CI: 1.2-5.4) and alcohol use disorders (OR = 2.8, 95%CI: 1.3-6.1) were associated with offspring SAD. Offspring’s reports of parental overprotection, rejection and lack of emotional warmth, but not parental reports of family functioning were associated with offspring SAD. Analyses of interaction of parental psychopathology and parental rearing indicated combined effects on the risk for offspring SAD. Conclusions. These findings extend previous results in showing that both parental psychopathology and parental rearing are consistently associated with the risk for offspring SAD. As independent and interactive effects of parental psychopathology and parental rearing may have already manifested in early adolescence, these factors appear crucial and promising for targeted prevention programs.

Hintergrund. In klinischen und epidemiologischen Untersuchungen wurden retrospektiv Assoziationen zwischen Angst- und Alkoholstörungen bestätigt. Bei Personen, die von beiden Störungen betroffen waren, fand man restrospektiv meist einen früheren Beginn der Angststörungen im Vergleich zu den Alkoholstörungen, was kausal im Sinne der Selbstmedikationshypothese interpretiert wurde. Diese konnte bisher nicht eindeutig bestätigt werden. Zur Aufklärung notwendige prospektive Untersuchungen, die Angststörungen auf diagnostischer Ebene erfassen, zwischen verschiedenen Angststörungen unterscheiden und sich auf Jugendliche beziehen, fehlen bisher. Fragestellung. Die Bedeutung von Angststörungen für die Entwicklung von erhöhtem Alkoholkonsum und Alkoholstörungen bei Jugendlichen und jungen Erwachsenen. Methodik. Die Analysen basieren auf den Daten der prospektiv-longitudinalen EDSP-Studie (Follow-Up: insg. 4 Jahre) mit einer epidemiologischen, repräsentativen Stichprobe von 3021 Personen im Alter zwischen 14 und 24 Jahre zu T0 aus München und Umland. Zur Erhebung von DSM-IV-Diagnosen wurde das M-CIDI verwendet. Ergebnisse. Primäre Panikstörungen, Panikattacken und Soziale Phobie erwiesen sich prospektiv als spezifische Prädiktoren für Beginn und Aufrechterhaltung von Alkoholproblemen. Umgekehrt waren Alkoholprobleme mit einem erhöhten Risiko für den Beginn von Sozialer Phobie und GAS assoziiert. Bezüglich DSM-IV Diagnosekriterien fanden sich phobische Ängste sowie Episoden intensiver Angst als Risikofaktoren für den Beginn von Alkoholproblemen. Vermeidungsverhalten war mit einem verminderten Risiko für nachfolgende Alkoholprobleme verbunden. Schlussfolgerungen. Maßnahmen zur Prävention von Alkoholproblemen können sich zielgruppenorientiert an Jugendliche mit Sozialer Phobie und Paniksymptomatik richten. Bei Patienten, die sich wegen Alkoholproblemen in Behandlung begeben, ist eine umfassende Diagnostik zur Identifikation zusätzlicher Angststörungen ratsam. / Background. Many clinical and epidemiological studies have documented significant cross-sectional comorbidities between anxiety disorders and alcohol use disorders. Analysis of retrospective age-of-onset reports suggests that the anxiety disorders often start earlier than the alcohol disorders. These data have often been interpreted in terms of a self-medication-model implying a causal mechanism. Overall, in former studies this model couldn't definitely be proofed. Prospective studies that follow a sample of adolescents into adulthood assessing different anxiety disorders on an diagnostic level are needed to confirm these associations. Methods. Baseline and four-year-follow-up data from the EDSP-Study, a prospective community survey of 3021 (2548 at follow-up) adolescents and young adults aged 14 to 24 years at baseline carried out in Munich, were used. DSM-IV anxiety disorders, alcohol use and alcohol use disorders were assessed with the M-CIDI. Results. While in retrospective analyses strong associations between nearly all anxiety disorders and alcohol problems, especially harmful use and dependence, were found, prospective analyses showed that only primary panic disorder, panic attack and social phobia are specific predictors of subsequent onset and persistence of alcohol problems. Contrary, primary alcohol problems were related to subsequent onset of social phobia and GAD. Considering the different DSM-IV-criteria, phobic anxiety as well as episodes of intensive anxiety were found to be risk factors for the following onset of alcohol problems. Avoidance behavior was associated with a lower risk for subsequent alcohol problems. Conclusions. Alcohol prevention programs could be directed to target groups with social phobia and panic. Patients with alcohol problems should carefully be screened for comorbid anxiety disorders. In order to prevent relapses the treating of social phobia and panic should be part of the therapy with comorbid alcohol patients.

No description available.

L’objectif de la présente thèse était de caractériser le sommeil d’un groupe clinique d’enfants et d’adolescents ayant un trouble d’anxiété comme diagnostic primaire et le comparer à un groupe témoin. Dans un premier temps, nous avons vérifié si le profil de la fréquence cardiaque nocturne des enfants et des adolescents pouvait être regroupé selon le diagnostic. Pour ce faire, la fréquence cardiaque nocturne de 67 adolescents anxieux et 19 sujets non anxieux a été enregistrée à l’aide d’un équipement ambulatoire. Les résultats de cette étude montrent que le profil de la fréquence cardiaque nocturne chez les enfants anxieux varie selon le diagnostic. Alors que les adolescents non anxieux montrent un profil de la fréquence cardiaque nocturne plat, on retrouve les associations suivantes chez les adolescents ayant un trouble anxieux : a) un profil croissant de la fréquence cardiaque chez les adolescents ayant un trouble d’anxiété de séparation; b) un profil décroissant de la fréquence cardiaque chez les adolescents ayant un trouble d’anxiété généralisé; c) un profil en forme de U chez les adolescents ayant un trouble d’anxiété sociale. De plus, une association significative a été observée entre le diagnostic et la présence de fatigue matinale. L’association d’un profil de la fréquence cardiaque nocturne avec un diagnostic d’anxiété suggère la présence d’une dysrégulation de la modulation chronobiologique du système nerveux autonome. Étant donné que le profil de la fréquence cardiaque nocturne s’exprime différemment selon le diagnostic, qu’en est-il de l’architecture du sommeil? Dans un deuxième temps, nous avons enregistré le sommeil en laboratoire d’un groupe clinique de 19 jeunes ayant un trouble d’anxiété comme diagnostic primaire, avec comorbidités et médication et comparé à 19 jeunes non anxieux. Les résultats de cette étude ont montré que les participants du groupe anxieux ont une latence au sommeil plus longue, une latence au sommeil paradoxal plus longue et une durée d’éveil plus longue lorsque comparé au groupe témoin. L’évaluation subjective de la qualité du sommeil chez le groupe d’adolescents anxieux montre que leur auto-évaluation reflète les valeurs enregistrées en laboratoire. Nous avons également observé chez le groupe anxieux une fréquence cardiaque moyenne plus élevée et un index plus élevé d’apnée-hypopnée, bien que non pathologique. Nous avons également observé une association positive entre l’anxiété de trait et l’indice d’apnée-hypopnée et la latence au sommeil, ainsi qu’une association positive entre l’anxiété manifeste et la latence au sommeil paradoxal. Ces résultats suggèrent que le sommeil chez cette population est altéré, que des signes d’hypervigilance physiologique sont présents et qu'une association existe entre ces deux paramètres. Finalement, dans la troisième étude de cette thèse, nous avons analysé l’activité cardiaque pendant le sommeil en utilisant les paramètres temporels et fréquentiels de la variabilité cardiaque chez un groupe clinique de dix-sept enfants et adolescents ayant un trouble d’anxiété comme diagnostic primaire avec comorbidité et médication, et comparé à un groupe non anxieux. Les résultats ont montré que les participants du groupe anxieux, lorsque comparés au groupe non anxieux, présentent des intervalles interbattements plus courts, un indice temporel de la variabilité cardiaque représentant la branche parasympathique moindre, une activité des hautes fréquences normalisées moindre et un ratio basse fréquence sur haute fréquence augmenté. Plusieurs corrélations ont été observées entre les mesures cliniques de l’anxiété et les mesures de la variabilité cardiaque. Ces résultats viennent ajouter à la littérature actuelle un volet descriptif clinique à ce jour non documenté, soit l’impact de l’anxiété pathologique chez un groupe clinique d’enfants et d’adolescents sur le processus normal du sommeil et sur la régulation de la fréquence cardiaque. En résumé, les résultats de ces trois études ont permis de documenter chez un groupe clinique d’enfants et d’adolescents ayant de l’anxiété pathologique, la présence d’une altération circadienne du profil de la fréquence cardiaque, d’une architecture altérée du sommeil ainsi qu’une dysrégulation du système nerveux contrôlant l’activité cardiaque. / The aim of this thesis was to characterize, in a clinical group of children and adolescents with anxiety disorder as a primary diagnostic, the sleep period and to compare it to a control group. Firstly, we have verified if the nocturnal sleep pattern of children and adolescents could be grouped by psychiatric disorders. Sixty-seven children and adolescents with anxiety disorders and nineteen non anxious match controls were monitored using ambulatory recording equipment. Results showed that nocturnal heart rate pattern of anxious adolescents would vary accordingly with the diagnosis. While non anxious adolescents exhibit a flat nocturnal heart rate pattern through the night, anxious participants showed the following associations: a) increased nocturnal heart rate pattern associated with separation anxiety disorder; b) decreased nocturnal heart rate pattern associated with generalized anxiety disorder; and c) U shape nocturnal heart rate pattern associated with social phobia. Moreover, a significant association was found between anxiety diagnosis and presence of morning fatigue. The association between nocturnal heart rate patterns with anxiety suggests that the circadian modulation of heart rate is dysregulated, but what about the sleep macrostructure? Secondly, we have monitored in a sleep laboratory a clinical sample of nineteen adolescents with pathological anxiety, comorbidity and medication, and compared it to nineteen non anxious match controls. Results showed that anxious participants had longer sleep latency, longer REM sleep latency and longer awake period during sleep when compared to control participants. Compared to control participants, anxious patients subjectively reported sleep disturbances, manifested objective sleep disorders and presented no adaptation to the laboratory environment. Moreover, higher nocturnal heart rate and higher apnea-hypopnea index were observed in anxious group when compared to non anxious group. Significant positive associations were observed between Trait anxiety and apnea-hypopnea index as well as for sleep latency while manifest anxiety was associated to REM sleep latency. Results suggest that sleep of children and adolescents with pathological anxiety is altered, that signs of physiological hypervigilance are observed and that both are associated. Following previous results, we have analyzed in a third study heart rate variability during nocturnal sleep using both, times and frequency domains in a clinical sample group of seventeen children and adolescents with anxiety disorder as primary diagnostic with comorbidity and medication. Results showed that anxious when compared to non anxious, had a shorter interbeat interval, and had lower rMSSD values, less high frequency in normalized units and higher low frequency/high frequency ratio. Correlations were observed between clinical anxiety scores and time and frequency domains of heart rate variability. These results add to the growing body of literature that pathological anxiety in a clinical group of children and adolescents impact on sleep process and heart rate regulation during sleep. Overall findings add to the growing body of recent clinical literature, a sleep alteration description of a clinical sample of children and adolescents. From the three studies of this thesis, results showed that circadian heart rate pattern is altered, that sleep architecture is altered, and that the time and frequency domain of nocturnal heart rate variability is altered in a clinical group of children and adolescents with pathological anxiety.

Pathologische Sorgen sind ungenau definiert. Für die Behandlungsplanung bleiben wichtige Fragen offen: Welche Merkmale sind für die Unterscheidung zwischen behandlungsbedürftigen und nicht behandlungsbedürftigen Sorgen relevant? Welche Art von Sorgen muss wie behandelt werden? Und: Welche Art von Sorgen gilt es eher zu akzeptieren? Wir machen praxisnahe Vorschläge dafür, wie Sorgen mittels einer einfachen Heuristik auch vom Patienten selbst als «pathologisch» identifiziert werden können. Im Sinne eines therapeutischen Arbeitsmodells ergeben sich differentielle Bearbeitungsstrategien, je nachdem, ob es sich um wichtige oder weniger wichtige, auf lösbare oder unlösbare Probleme bezogene sowie angemessene oder überzogene Sorgen handelt. Das vorgestellte Arbeitsblatt zu den Sorgen soll vor allem die wahrgenommene Kontrolle des Patienten stärken und die Psychoedukation zur Generalisierten Angststörung erleichtern. / Pathological worries have not yet been clearly defined. As a consequence, practically relevant questions remain open: Which characteristics distinguish worries relevant for treatment from those which are not? What kind of worries has to be treated in which way? And: What kind of worries is rather to be accepted? We propose a simple rationale which helps the therapist and the patient to identify pathological worries. According to this working model, different treatment strategies result depending on whether worries are central or not, whether they relate to a problem which can be solved or not, and whether they seem proportionate or exaggerated. The presented worksheet is meant to strengthen the perceived control of the patient and to help facilitate psychoeducation for generalised anxiety disorder. / Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.

Background: Worry exposure (WE) is a core element of cognitive-behavioral treatment for generalized anxiety disorder (GAD). Its efficacy as a stand-alone treatment method (without further cognitive-behavioral therapy interventions) has never been tested.We aimed to examine whether WE alone is as efficacious as the empirically supported stand-alone treatment for GAD, applied relaxation (AR). Methods: In a randomized controlled study, 73 outpatients meeting DSM-IV criteria for GAD as primary diagnosis were allocated to either WE or AR or a waiting list control group; in a 2nd randomization procedure the waiting list subjects were reallocated to WE or AR. The treatment was manualized (15 sessions with WE or AR), included 6-month and 1-year follow-ups, as well as last observation carried forward and completer analyses, and was controlled for allegiance effects.The Hamilton Anxiety Rating Scale and the State-Trait Anxiety Scale were used as primary outcome measures. Self-report scales of anxiety, worrying and depression including negative metacognition about worrying and thought suppression served as secondary outcome measures. Results: The dropout rate was moderate. The pre-/posttreatment effects were high for the Hamilton Anxiety Rating Scale (standardized mean difference >1) and for the State-Trait Anxiety Inventory (standardized mean difference >0.87). The proportion of patients reaching high end state functioning was 48% (WE) and 56% (AR). WE and AR did not differ with regard to dropout rate or treatment effects. The treatment effects were stable at 6 month and 1 year follow-up. Conclusion: This is the first study to show that a stand-alone exposure in sensu technique – WE – is efficacious in the treatment of GAD. Both AR and WE seem to represent effective principles of change in GAD. / Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.