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Beginning with the eighties, a paradigm-change concerning anxiety disorders has taken place in considerable parts of psychiatry. Anxiety disorders are no longer regarded as consequences of conflicts and ineffective defences or as concomitants of other psychiatric disorders but rather as disorders of their own. This resulted in a modified outlook on anxiety disorders focusing on the acute panic attack (Panic disorder) instead of focusing on chronic anxiety (Anxiety neurosis). This paper reviews recent empirical studies concerning classification, pathogenesis, and therapy of anxiety disorders, i.e. after introduction of the concept of Panic disorder. Epidemiological studies could demonstrate that in western countries anxiety disorders account for the most frequent psychiatric disorders with prevalence rates of 2.0% to 4.7%. Panic disorders show prevalence rates of 0.4% to 1.1%. Results of recent follow-up studies indicate a favorable course for outpatients and an unfavorable course for inpatients with anxiety disorders. Family studies reported on positive familial loading for Panic disorder but not for Agoraphobia and Generalized anxiety disorder. A twin study found higher concordance rates for panic attacks and Agoraphobias in monozygotic twins than in dizygotic twins. Pharmacological provocation studies with lactate infusion, CO2-inhalation, and administration of Caffeine, Yohimbine, Isoproterenol showed a higher vulnerability of patients with Panic Disorder as compared to healthy controls. However, all studies display methodological short-comings and could be interpreted differently as to the concept of a biologically determined vulnerability. Provocation studies using inverse Benzodiazepine-agonists dealt only with healthy probands. Whereas life events play a rather unimportant role für the pathogenesis of anxiety disorders, recent studies point to the influence of cognitive processes and personality variables for the pathogenesis of anxiety disorders. Concerning treatment of anxiety disorders and especially of panic disorders, pharmacological studies as well as studies of behavioural therapy indicate very good results for acute treatment and good results for behavioural therapy with respect to one to four year follow-up studies. Recently, combined drug and psychotherapy gains growing interest. Conclusions are drawn with respect to the usefulness of the new classification, i.e. after the introduction of Panic disorder as a diagnostic category, and references are given for further research strategies.

On the point of anxiety states, behavioural sciences have only recently been provided with sufficient operational definitions of clinical concepts to enable us to start working on the construction of valid models for the different disorders. Panic attacks are defined as attacks manifested by discrete periods of apprehension or fear, concomitant with at least four marked vegetative sensations, as described in the DSM-III. Several interventions have proved to be able to mimic experimentally such episodes in vulnerable patients, providing the researcher with valuable models for panic research such as the lactate infusion technique, the single CO2 inhalation model and, to a lesser extent, the hyperventilation provocationtest. The study of these models may be a major contribution to a better understanding of panic anxiety, both from a biological and behavioural point of view. Biological observations of those models point to pH changes and ionic shifts as a physiological concomitant in the genesis of experimentally induced panic, and suggests that hypersensitive chemoreceptive structures of the CNS may be implicated. As to the behavioural aspects of the models, there is strong evidence for the ancient phobophobia, or "fear of fear" idea, which may explain the invaldating recurrence of panic attacks.

The currently available empirical findings lead us to assume that various forms of anxiety disorders--such as generalised anxiety syndrome or panic disorder--are based on different pathophysiological mechanisms with varying involvement of different neurotransmitter systems. We must bear in mind that whereas the disturbance of a transmitter may predominate--such as the disturbance of the noradrenalin system in panic disorder and that of the GABA-ergen system in generalised anxiety--on the other hand the transmitter systems are mutually interlinked, so that an isolated disturbance of a system is very unlikely. However, to the present date it has not been possible to give a definite biochemical characterisation of a certain disease pattern, such as that of panic disorder. Likewise, no unequivocal conclusions can be drawn in respect of cerebral localisation. Nevertheless, results obtained in animal experiments suggest that in panic disorder certain brain areas like e.g. the locus ceruleus may be affected. Future hopes rest in developing more specific drugs that selectively change a transmitter system and on new techniques such as positron emission tomography enabling a better insight into the mode of functioning of the brain. New possibilities seem to be offered also by defining a predisposition via molecular-genetic methods.