English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Background:  Alexithymia, an inability to recognise one’s emotions, has been associated with trauma-exposure and posttraumatic stress disorder (PTSD). Previous research suggests involvement of the oxytocin system, and socio-emotional neural processes. However, the paucity of neurobiological research on alexithymia, particularly in trauma-exposed populations, warrants further investigation. Objective:  Explore associations between alexithymia, endogenous oxytocin levels, and socio-emotional brain function and morphometry in a trauma-exposed sample. Method:  Dutch trauma-exposed police officers with ( n  = 38; 18 females) and without PTSD ( n  = 40; 20 females) were included. Alexithymia was assessed with the Toronto Alexithymia Scale (TAS-20). Endogenous salivary oxytocin was assessed during rest, using radioimmunoassay. Amygdala and insula reactivity to socio-emotional stimuli were assessed with functional MRI, amygdala and insula grey matter volume were derived using Freesurfer. Results:  Alexithymia was higher in PTSD patients compared to trauma-exposed controls ( F (1,70) = 54.031,  p  &lt; .001). Within PTSD patients, alexithymia was positively associated with PTSD severity ( ρ (36) = 0.497,  p  = .002). Alexithymia was not associated with childhood trauma exposure ( β  = 0.076,  p  = .509), police work-related trauma exposure ( β  = −0.107,  p  = .355), oxytocin levels ( β  = −0.164,  p  = .161), insula ( β  = −0.170,  p  = .158) or amygdala ( β  = −0.175,  p  = .135) reactivity, or amygdala volume ( β  = 0.146,  p  = .209). Insula volume was positively associated with alexithymia ( β  = 0.222,  p  = .016), though not significant after multiple testing corrections. Bayesian analyses supported a lack of associations. Conclusions:  No convincing neurobiological correlates of alexithymia were observed with any of the markers included in the current study. Yet, the current study confirmed high levels of alexithymia in PTSD patients, independent of trauma-exposure, substantiating alexithymia’s relevance in the clinical phenotype of PTSD.

How does it feel? An exploration of neurobiological and clinical correlates of alexithymia in trauma-exposed police-officers with and without PTSD