Cognitive and behavioural processes may constitute a risk for onset and persistence of depression. People who become depressed frequently show enduring negative cognitions which predispose them to depression. In addition, interpersonal processes are supposed to contribute to the etiology and maintenance of depression. Depression-prone persons are presumed to display deficient or problematic social behaviours that elicit negative reactions in others, finally resulting in withdrawal by family and friends.

About 60% of human communication is non-verbal. An ethological approach may therefore contribute to reveal behavioural and cognitive vulnerability factors for depression onset or persistence. Various studies support this presumption: High levels of patients' observed behaviour indicating involvement in the interaction between depressives and clinicians at admission are related with persistence of depression.

According to interpersonal theories on depression, the type of interaction between depression-prone subjects and their social environment plays a causal role in the development and course of depression (e.g. Coyne et al.). So far, interpersonal theories have been tackled mostly by psychometrical methods. However, non-verbal behaviour plays an important role in human social interactions. It is assumed that 60-65% of human communication is non-verbal. Ethological observations have shown that non-verbal interpersonal behaviour of depressed subjects, as assessed prior to treatment, is related to treatment-response or subsequent course of depression. These results are in line with an interpersonal approach of depression.

The purpose of this article is to give a comprehensive review of biological theories about the development of panic disorder.

Noradrenergic, serotonergic and GABA-ergic models of panic disorder are discussed, together with the role of peptides and neuroanatomical hypotheses.

The conclusion is that there is no unitary biological explanation of panic disorder.

An intergrative bio-psycho-social model seems for the moment the most usefull.

A review is given of the neuropsychological conceptualizations of aphasia and apraxia in SDAT. In the beginning of this century localisationism was prevailing. Later, developmental and cognitive psychology gave an important impetus to reconsider these symptoms in an holistic framework. More recently, since the application of new brain imaging techniques, there is a revival of localizing conceptualizations.

Decades of research into the etiology of schizophrenia on a phenotypic level, i.e. studies of neuroanatomy, neuropathology, neurophysiology and other areas such as immunology have yielded only fragmentary results. A contribution of genetic factors, has been consistently shown, however, beginning with E. Kraepelin's pioneering studies at the turn of the century. Evidence has accumulated from family-, twin-, and adoption studies. Identical twins have a 48% risk of developing schizophrenia if one of them is affected. In contrast, a 17 % risk is reported for nonidentical twins. These rates are similar to other complex genetic disorders such as diabetes, hypertension and asthma. Advances in the genetic analysis of complex traits as well as progress in the Human Genome Project should provide a basis for uncovering the molecular causes of schizophrenic disorders and for investigating the neuropathology of this individually and socially devastating neuropsychiatrie disorder. There is no doubt, that discovery of the genetic variation associated with the illness would help in identifying specific targets for development of more effective, targeted treatments.