Emotional numbing in PTSD is associated with lower amygdala reactivity to pain

Nachshon Korem, Or Duek, Ziv Ben-Zion, Antonia N. Kaczkurkin, Shmuel Lissek, Temidayo Orederu, Daniela Schiller, Ilan Harpaz-Rotem, Ifat Levy

Research output: Contribution to journalArticlepeer-review

Abstract

Posttraumatic stress disorder (PTSD) is associated with altered pain perception, namely increased pain threshold and higher pain response. While pain consists of physiological and affective components, affective components are often overlooked. Similar patterns of increased threshold-high response in PTSD were shown in response to emotional stimuli, i.e., emotional numbing. As both emotional numbing and pain processing are modulated by the amygdala, we aimed to examine whether individuals diagnosed with PTSD show lower amygdala activation to pain compared with combat controls, and whether the amygdala responses to pain correlates with emotional numbing. To do so, two independent samples of veterans (original study: 44 total (20 PTSD); conceptual replication study: 40 total (20 PTSD)) underwent threat conditioning, where a conditioned stimulus (CS+; visual stimulus) was paired with an unconditioned stimulus (US; electric-shock). We contrasted the amygdala activity to the CS + US pairing with the CS+ presented alone and correlated it with emotional numbing severity. In both samples, the PTSD group showed a robust reduction in amygdala reactivity to shock compared to the Combat Controls group. Furthermore, amygdala activation was negatively correlated with emotional numbing severity. These patterns were unique to the amygdala, and did not appear in comparison to a control region, the insula, a pivotal region for the processing of pain. To conclude, amygdala response to pain is lower in individuals with PTSD, and is associated with emotional numbing symptoms. Lower amygdala reactivity to mild pain may contribute to the “all-or-none” reaction to stressful situations often observed in PTSD.

Original languageEnglish (US)
Pages (from-to)1913-1921
Number of pages9
JournalNeuropsychopharmacology
Volume47
Issue number11
DOIs
StatePublished - Oct 2022

Bibliographical note

Funding Information:
This work was supported by NIH R01MH105535 to DS and IHR, CSRD CX001538 grant to IHR, NIH R01MH118215 to IL, and NSF BCS-1829439 to IL. DS is supported by the NIMH (R01MH122611, R01MH123069) and the Misophonia Research Fund. Replication study was originally supported by NIMH grant MH-080130 to SL.

Publisher Copyright:
© 2022, The Author(s), under exclusive licence to American College of Neuropsychopharmacology.

PubMed: MeSH publication types

  • Journal Article
  • Research Support, Non-U.S. Gov't
  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.

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