Neurocognitive correlates of the varied domains of outcomes at 20 year follow-up of first-episode psychosis.

Little is known about long-term outcomes of the first episode of psychosis (FEP) other than in the symptomatic domain. We hypothesised that cognitive impairment is associated with poorer multi-domain outcomes at a long-term follow-up of FEP patients. We followed-up 172 FEP patients for a mean of 20.3 years. Ten outcome dimensions were assessed (symptomatic, functional and personal recovery, social disadvantage, physical health, suicide attempts, number of episodes, current drug use, chlorpromazine equivalent doses (CPZ), and schizophrenia/schizoaffective disorder final diagnosis). Cognition was assessed at follow-up. Processing speed and verbal memory deficits showed significant associations with poor outcomes on symptomatic, social functioning, social disadvantage, higher number of episodes, and higher CPZ. Significant associations were found between visual memory impairments were significantly associated with low symptomatic and functional recovery, between attentional deficits and a final diagnosis of schizophrenia/schizoaffective disorder, and between social cognition deficits and poor personal recovery.Lower cognitive global scores were significantly associated with all outcome dimensions except for drug abuse and physical status. Using multiple outcome dimensions allowed for the inclusion of the patients' perspective and other commonly neglected outcome measures. Taken together, cognitive impairment in FEP patients is strongly related to poor performance on several outcome dimensions beyond symptomatic remission.

Neurobiología de la depresión / Neurobiology of depression

El modelo neurobiológico en el que durante muchos años se han basado la etiología, y por lo tanto el tratamiento de la depresión, comprendía básicamente alteraciones en el funcionamiento de los neurotransmisores, o en los receptores de los mismos. Sin embargo, investigaciones recientes han transformado el escenario de la patofisiología de la depresión, implicándose distintos niveles y sistemas, tanto nerviosos como endocrinos e inmunes, e incluso celulares, moleculares y genéticas. Desde esta nueva perspectiva se pueden entender mejor los síntomas de la depresión y muchas de sus alteraciones neurobiológicas. El presente trabajo pretende integrar de una manera global los distintos mecanismos biológicos que se han relacionado con la etiología de la depresión, para permitir un nuevo abordaje conceptual de los trastornos depresivos y abrir nuevas posibilidades terapeúticas en el futuro (AU)

[Neurobiology of depression]. / Neurobiología de la depresión.

During decades, both aetiology and treatment in Depressive Disorders relied on neurotransmitters' physiopathology or on abnormalities 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, immune and endocrine systems seems to interact among themselves and to influence on clinical manifestations of illness. Moreover, dysregulations on lower levels, such as intracellular and genetic systems might cause anomalies in protein expression, and in consequence might modulate receptors' disfunction and disturbances at the intramolecular level of signal transmission. The above disturbances 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.