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Background: It has been reported that lack of insight is significantly associated with cognitive disturbance in schizophrenia. This study examines the longitudinal relationships between insight dimensions and cognitive performance in psychosis.

The diagnosis of cycloid psychosis has a long tradition in European psychiatry. However, it has been poorly assimilated within the DSM IV and ICD-10 diagnostic systems. Leonhard set the basis for the current conceptualization of the disorder, and Perris and Brockington developed the first operational diagnostic criteria. However, the two conceptualizations of the disorder are not the same and differ across a number of meaningful variables. Cycloid psychosis is a useful concept in that it possesses both clinical and predictive validity. Despite the high prevalence of mood symptoms and syndromes, cycloid psychosis does not equal schizoaffective disorder. Although a substantial body of evidence suggests that cycloid psychosis differs meaningfully from typical schizophrenia, it is less clear whether it differs from major mood disorders or represents an independent nosological entity. The existence of putative subtypes is also likely, and the differentiation between affective and nonaffective subtypes has received some support.

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During decades, both aetiology and treatment in Depressive Disorders relied on neurotransmisors' physiopathology or on abnomalities in their receptors function. However, recently evidences from research on neurobiological grounds suggest that there are multiple and complex systems involved in the pathophysiology of Depressive Disorders. Several neurobiological structures, such as the neural, inmune and endocrine systems seems to interact among themselves and to influence on clinical manifestations of illness. Moreover, disregulations on lower levels, such as intracellular and genetic systems might cause anomalities in protein expression, and in consequence might modullate receptors' disfunction and disturbances at the intramolecular level of signal transmission. The above distrubances at different levels of complexity are finally integrated within the frame of most recent theoretical approaches to Depressive Disorders. Specifically, recent theories implicating neuronal plasticity and survival-death cell mechanisms are described. The aim of this review is to integrate recent evidence on pathophysiological mechanisms of Depressive Disorders. New lines of treatment based upon these 'new pathophysiology' of depression will be wellcome.