Philadelphia, September 12, 2018 – A new report published in European Psychiatry identified a significant association between childhood adversity and impaired social cognitive functioning among adults diagnosed with major psychiatric disorders. Through a comprehensive review of all research conducted to date, the investigators established that a traumatic early social environment frequently leads to social cognitive problems and greater illness severity for individuals with schizophrenia, bipolar disorder, borderline personality disorder, major depressive disorder, or post-traumatic stress disorder.
"Early childhood neglect, abuse, and/or trauma puts patients at greater risk for developing cognitive impairments that will later affect social perception and interaction, a core aspect of disability in major psychiatric disorders," explained lead investigator, Gary Donohoe, MPsychSc, DClinPsych, PhD, Centre for Neuroimaging and Cognitive Genomics, National University of Ireland, Galway, Ireland.
Deficits in social cognitive function are a hallmark feature of major psychiatric disorders resulting in impaired social and occupational functioning, specifically with regard to emotion recognition and regulation, theory of mind (the ability to attribute mental states to oneself and others), attributional style, and social perception. Traumatic childhood experiences — such as emotional and physical abuse and neglect, early loss of caregivers, and insecure attachment styles — are frequently reported in as high as 85 percent of patients with various psychiatric disorders.
These findings are relevant to gain a better understanding the mechanisms between a traumatic early social environment and subsequent social cognitive problems and increased illness severity for a range of major psychiatric disorders in adulthood. The first three years of life are a very sensitive period for the development of attachment relationships, and exposure to traumatic events during this time has irreversible effects on subsequent cognitive, social, and emotional development. The link between childhood adversity and insecure attachment is supported by a number of previous studies. Once a dysfunctional attachment pattern is formed in childhood, it tends to persist later in life and can cause misperceptions of others' intentions and beliefs. Heightened threat vigilance can distract abuse victims from processing peripheral cognitive and social information, and the lack of stable, positive role models can interfere with their ability to recognize and respond to emotional cues.
The investigators hope that the study will guide future public health efforts to develop clinical interventions that reduce the consequences of childhood adversity. "With a better understanding of the connections between early trauma and later deficits, mental health clinicians may be able to develop strategic interventions that ameliorate patients' disabilities and improve their quality of life. The fact that these deficits are not generally improved by antipsychotic medication makes social cognition an important treatment target and the development of a causal working model of the deficits of crucial importance," noted Prof. Donohoe.
The study, funded by the European Research Council and Science Foundation Ireland, involved a systematic review of the published literature to provide a comprehensive picture of current research. This included the assessment of more than 2,650 published papers on the topic that were identified using the PubMed and PsycINFO databases. Of these, 25 research articles were found to meet the study's strict criteria and were included in the review. The investigators recommend additional research to model the relationship between early adversity and genetic risk that contributes to social cognitive development. Understanding the mechanisms by which neurocognitive and biological factors come into play is also an important subject for future study.
###
Media Contact
Damon Mastandrea
[email protected]
215-239-3555
@elseviernews
http://www.elsevier.com
http://dx.doi.org/10.1016/j.eurpsy.2018.06.006
