Connecting the dots: Neurodevelopmental trauma and adult psychosis

Longitudinal research has shown that a large proportion of patients who experience psychiatric disorders in adulthood were already showing symptoms in their adolescence.1 In addition, trauma and adverse life experiences early in life confer an increased risk for psychosis.2 In this session, two speakers (Prof Mary Cannon, Ireland and Dr Michael Bloomfield, UK) discussed the links between early trauma and the development of psychosis, and another two (Prof Paul Lucassen, The Netherlands, and Dr Daniella Dwir, Switzerland) reviewed data on some of the brain mechanisms that may be involved in this pathophysiology.

Severe clinical phenotype following developmental trauma

Developmental risk factors for psychiatric disorders include child poverty, and childhood trauma and adversity. These traumas are associated with a more severe clinical phenotype, with severe symptoms and hallucinations with content related to trauma memories. There is also an impaired response to standard treatments, more re-admissions to hospital, and less good engagement with therapeutic services. Therefore, it is important to mitigate the effects of these traumas if at all possible.

Patients who have experienced developmental trauma also show lower cortical thickness and smaller hippocampal volume than those who have not. Brain substrates of trauma include the amygdala, hippocampus, prefrontal cortex and striatum, and there are different windows during development, in which those brain regions are more susceptible to harm.3 Changes in vulnerable brain areas, as a result of developmental trauma, may lead to attentional bias towards threatening emotional stimuli and impaired reinforcement learning.

 

Effects on neurogenesis and oxidative stress may play their part

In the brain, early life experiences may have direct effects on neurogenesis. This is known to be reduced by chronic stress, and this is implicated in the reversible loss of hippocampal volume in depression.4 In animal studies, prenatal stress results in a reduction in neurogenesis over time. This has consequent detrimental effects on hippocampal behavioural tasks.5

Early life experiences may have direct effects on adult neurogenesis

Early traumatic experiences are also linked with oxidative stress in the brain and periphery, and this has been associated with smaller hippocampal volumes.6 Oxidative stress can also lead to impairment of parvalbumin interneuron maturation. This, in turn, leads to impaired neural synchronization, disrupted information processing and integration leading to the symptoms and cognitive deficits associated with schizophrenia.7

 

The significance of psychotic experiences

An early sign of psychotic disorders, which is also associated with trauma and adverse life events, is the presence of psychotic experiences (such as hearing voices, the feeling of being watched, followed or under someone else’s control, etc.).8,9 Interventions to reduce or stop traumas, such as bullying, were also able to reduce the incidence of psychotic experiences.10 Therefore, there is a possibility that early steps to mitigate or prevent adverse life experiences will reduce the onset of psychiatric disorders at a later date.

Reducing trauma exposure can reduce psychotic experiences

Another possible point of intervention is in the psychological factors that mediate adverse experiences and their transformation into psychotic events. Thus, interventions aimed to increase people’s self-esteem, or to improve parental support and coping styles could all reduce the risk of experiencing psychotic experiences following adverse life events, and therefore the risk for psychiatric disorders.11,12  

Intervening early makes primary prevention a possibility

This points to possibilities for primary and secondary prevention strategies to prevent people from developing, and help them manage, the early signs of serious psychiatric disorders.

 

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Our correspondent’s highlights from the symposium are meant as a fair representation of the scientific content presented. The views and opinions expressed on this page do not necessarily reflect those of Lundbeck.

References
  1. Kim-Cohen J et al. Arch Gen Psychiatry 2003 Jul;60(7):709–17.
  2. Coughlan H and Cannon M. Br J Psych Advances 2017;23(5):307–15.
  3. Teicher MH et al. Nature Reviews Neuroscience 2016;17:652–66
  4. Lucassen PJ et al. Eur Neuropsychopharmacol 2010;20(1):1–17.
  5. Lemaire V et al. PNAS 2000; 97 (20): 11032–7
  6. Alameda L et al. PNAS 2018;115 (49):12495–500
  7. Steullet P et al Schizophr Res 2016;176(1):41–51.
  8. van Os J et al. Psychol Med 2009 Feb;39(2):179–95.
  9. Kelleher I et al. Br J Psychiatry 2012 Jul;201(1):26–32.
  10. Kelleher I et al. Am J Psychiatry 2013;170(7):734–42
  11. Healy C et al. J Child Psychol Psychiatry 2019;60(11):1164–73
  12. McMahon EM et al. Psychol Med 2020;Feb 6:1-9.
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