Stressful life events and first-episode psychosis

Abstract

[eng] Nowadays, advances in affective and social neuroscience have shown how the exposure to environmental factors has an impact on the structure and functioning of the brain being thus, active agents in the formation of an individual’s level of vulnerability. There is an increasing interest in the influence of stress on many diseases including a first-episode psychosis (FEP). From the stress-vulnerability model (Zubin & Spring, 1977) to the current models of neural diathesis-stress (Pruessner et al., 2017), schizophrenia is conceptualised as an episodic disorder in which there is vulnerability and stress due to biological and/or environmental factors. This suggests that patients are likely predisposed to manifesting psychotic episodes induced by the impact of precipitating factors, such as stressful life events (SLEs). In FEP, the role of stressors, specifically SLEs, as predisposing factors or adjuvants to the onset of the disease is relevant. These events are circumstances that occur in the lives of people with an identifiable beginning and end which have the potential to alter their current mental or physical status. However, there are very few studies on SLEs in patients with schizophrenia - and even fewer in patients with FEP-, thereby emphasising the need for such studies. SLEs can be treated as prodromal events, which together with other events, contribute to the appearance of later psychotic symptomatology. Indeed, it is likely that the diversity of environmental factors associated with schizophrenia may be linked to an equal number of different underlying mechanisms. Several studies have evaluated the role of SLEs, but most of the studies include these events as trauma, what makes their research and evaluation more difficult and complicated. This thesis was aimed at achieving adequate and effective early intervention in psychotic disorders since: i) in general, few studies have specifically evaluated SLEs; ii) no studies have analysed the age of onset of FEP in relation to SLEs; iii) no studies have been found about gender differences, family history and psychotic symptomatology in relation to SLEs; and iv) no instruments are available to assess SLEs along the life cycle. The main objective of this thesis was to evaluate the relationship between SLEs and the development of FEP. This objective was developed under three specific objectives: 1) to systematically review the literature available on SLEs and FEP, 2) to evaluate the impact of SLEs and the influence of sociodemographic and clinical variables on the appearance of FEP, and 3) to validate an instrument to measure SLEs in FEP and in a healthy population. The data obtained in this thesis provide more in depth knowledge regarding SLEs and their evaluation and detection as well as the relationship of these events with clinical variables and symptoms in a sample of patients with FEP and healthy controls. The objective of identifying SLEs across the stress-vulnerability model psychosis phenotype continuum may provide insights into the aetiology of this disorder and may lead to the development of strategies for its prevention and treatment. We provide further corroboration that rather than being a correlate of frank psychosis, the variability of SLEs may play an important role in FEP populations and this is of great relevance to the practice of professionals dedicated to detecting, caring for, and treating people with this disease. The work presented in this thesis is framed within the stress-vulnerability model and the clinical staging model, which considers the phenotypic continuum reflecting a shared interactive set of diathesis, psychosocial and sociocultural factors. Currently, few studies have evaluated SLEs in these sample types and there is a need to obtain more in depth information on the influence of SLEs in these populations in which genetics and stress play a relevant role.

[cat] Actualment, els avenços en la neurociència afectiva i social han demostrat com l’exposició als factors ambientals influeix en l’estructura i la funció del cervell, essent agents actius en la formació del nivell de vulnerabilitat de l’individu. A més, hi ha un interès creixent en la influència de l’estrès en moltes malalties, incloent un primer episodi psicòtic (PEP). Des del model de vulnerabilitat-estrès (Zubin i Spring, 1977) fins als models actuals de diàtesi- estrès neural (Pruessner et al., 2017), l’esquizofrènia es conceptualitza com un trastorn episòdic en què hi ha vulnerabilitat i estrès a causa de factors biològics i/o ambientals. Això suggereix que probablement els pacients estiguin predisposats a manifestar episodis psicòtics induïts per l’impacte dels factors precipitants, com els esdeveniments vitals estressants (EVEs). En el PEP, és rellevant el paper dels estressors, específicament EVEs, com a factors predisponents o adjuvants a l’aparició de la malaltia. Aquesta tesi tenia com a objectiu aconseguir una intervenció primerenca adequada i efectiva en trastorns psicòtics ja que: i) en general, pocs estudis han avaluat específicament els EVEs; ii) cap estudi ha analitzat l’edat d’aparició de PEP en relació amb els EVEs; iii) no hi ha estudis sobre diferències de gènere, historia familiar i simptomatologia psicòtica en relació amb els EVEs; i per últim, iv) no hi ha instruments disponibles per avaluar els EVEs durant el cicle vital. L’objectiu principal d’aquesta tesi va ser avaluar la relació entre els EVEs i el desenvolupament del PEP. Aquest objectiu es va desenvolupar en tres objectius específics: 1) revisar de forma sistemàtica la literatura disponible dels EVEs i PEP, 2) avaluar l’impacte dels EVEs i la influència de les variables sociodemogràfiques i clíniques sobre l’aparició de PEP, i 3) validar un instrument per mesurar els EVEs en pacients amb PEP i en població sana. Les dades obtingudes en aquesta tesi proporcionen un coneixement més profund sobre els EVEs i la seva avaluació i detecció, així com la relació d’aquests esdeveniments amb variables i símptomes clínics en una mostra de pacients amb PEP i controls sans.