Causes:
Anxiety disorders are complex disorders. Environmental and genetic factors equally contribute to their pathogenesis. In the first half of the last century, on the basis of Freud's concept of anxiety neurosis, environmental factors such as life events in childhood and adolescence have been stressed as pathogenetic factors. They include separation from parents or spouses by death or divorce, experiences of physical or sexual violence and physical illness.
Based on Klein's observation that some forms of anxiety neurosis can be successfully treated by antidepressants, biological factors have been given more attention in the second half of the last century. Twin and family studies provide evidence for a major contribution of genetic factors. Linkage and association studies point to candidate loci such as chromosomes 13q and 22q as well as candidate genes such as serotonergic and noradrenergic genes. Genomewide association studies, due to their hypothesis-free approach, will help to identify new genes and new pathophysio-logical pathways.
The contribution of each factor, however, will be minor and explain only a few percent of the variance. Research efforts such as the DFG-funded special research network TRR58 on “Fear, Anxiety and Anxiety Disorders” utilizing endophenotypes (imaging genomics, pharmacogenomics) as well as animal models (knockout mice) will enhance our understanding of the complex interplay between environmental and genetic factors in the context of fear and anxiety networks including among others the amygdale and the prefrontal cortex.
Diagnosis:
Anxiety disorders like other mental disorders are defined as categories. IDC-10 and DSM-IV differentiate panic disorder with and without agoraphobia, generalized anxiety disorder, social phobia and specific phobia. Sometimes and in particular in the American literature post-traumatic stress disorder and obsessive-compulsive disorder are also added to the anxiety disorders although they show clearly distinct features from the other core anxiety disorders. Diagnosing an anxiety disorder warrants careful exclusion of somatic disorders imitating anxiety disorders. These include hyperthyreosis, certain arrhythmias, epilepsies and vestibular disorders among others. In addition to a careful physical examination therefore an electrocardiogram, an electroencephalogramm and a routine blood test including thyroid parameters should be performed. Depending on the results further tests such as a 24hour electrocardiogram, a 24 hour electroencephalogram, a cCT and/or a cMRT and a drug screening may become necessary. Occasionally, a real comorbidity may exist between anxiety disorders and certain somatic disorders such as arrythmias and asthma bronchiale. As anxiety may be a symptom also in other mental disorders, uni-as well as bipolar depressive disorders and somatoform disorders in particular have to be considered as alternative diagnoses. As with somatic disorders there may be true comorbidity with these disorders and also secondary substance abuse disorders which will effect treatment strategies. Structured interviews such as the SCID or the CIDI may be helpful in differentiating them. Rating scales such as the HAMAS or the PAS allow to semiquantitatively define the severity of the anxiety disorder.
In addition to establishing the categorical diagnosis it is important to define personality, cognitive and coping features of the individual patient as they will be important in designing an individually tailored therapy. Equally important are informations on the present life situation and the personal history (life events) in particular with regard to the nature of relations to family members as they are also important for designing the therapy.
Treatment:
As in some anxiety disorders such as panic disorder the patient has a somatic concept of the disorder based on its predominantly somatic symptoms, the first and most important treatment step is to develop a common psychosomatic concept of the etiopathogenesis of the disorder. Helpful models are the stress-vulnerability and the anxiety circle models. The need to spend enough time for this step cannot be overstressed.
Once this has been achieved, the therapy of choice in the treatment of anxiety disorders today is cognitive behavioural therapy. Numerous studies have proven its efficacy and numerous manuals for the individual anxiety disorders have been developed. The core element seems to be exposure to the fear inducing subject, object or situation. Research efforts such as the BMBF-funded PanicNet focus on the question if this is indeed so, and if yes, which form of exposure is more effective. Exposure in sense in generalized anxiety disorder or in sensu in agoraphobia. Modifications with a greater focus on cognitive strategies and a gradual exposure have to be applied in the elderly and the case of true comorbidity with certain somatic disorders. Cognitive behavioural therapy may be administered as more intensive individual therapy or as less intensive group therapy. The latter may be a good complement in particular in the case of social phobia. In some instances, e.g. blood-injury phobia additional treatment elements may be necessary. Psychodynamic therapy elements may be helpful in secondary prevention.
Among pharmacological approaches, treatment with selective serotonergic antidepressants is considered the treatment of choice. As, however, they may cause a worsening of symptoms prior to symptom reduction, their medication must be preceded by a careful information of the patient of their undesired effects. In general, in comparison with the treatment ofdepressions, uptitration should be slower and the maintenance dose lower. In particular in the case of comorbidity with depression, sedating antidepressants may be helpful. The use of benzodiazepines should be restricted to emergency situations because of their liability to the development of abuse and dependence. High-potency typical antipsychotics should not be administered because of the risk of tardive dyskinesia. A matter of controversy over the years has been the comparative efficacy and the combination of cognitive behavioural psychotherapy and pharmacotherapy with antidepressants. While convictions are strong, data are few. Those which exist seem to indicate that while pharmacotherapy has a faster, psychotherapy has a longer-lasting effect. The combination, if necessary in severe cases, seems to have advantages by combining a faster effect without compromising a long-lasting effect. Questions like these are topics of discussion of committees for treatment guidelines such as the S3-guideline currently being developed in Germany. Nevertheless, there seems to be emerging a consensus that while effective in many cases, cognitive behavioural therapy with exposure as core element may have to be complemented in severe cases by other therapy elements individually tailored to the individual patient.
