ABSTRACT
Background: The COVID-19 pandemic has had profound impacts on people worldwide. Previous studies have shown that fear learning, extinction, recall, and contextual information processing involve the activation of emotion and sensory brain systems, which can be modified. However, it remains unclear whether brain functions associated with these processes have been altered over the pandemic period. Methods: We compared pre- and peri-pandemic brain activation during a fear-associated learning task (FALT) using previously collected data. The participants were divided into two groups: the pandemic group (n = 16), who completed a baseline FALT before the pandemic and repeated the task during the pandemic, and the non-pandemic group (n = 77), who completed both sessions before the pandemic began. Results: Compared with the non-pandemic group, the pandemic group exhibited significant decreases in brain activation from baseline to follow-up assessments, including activation in the brainstem during early fear learning, the posterior thalamus/hippocampus during late extinction, and the occipital pole during late recall phases for contextual processing. Furthermore, activations associated with retrieving safety cues were reduced in the posterior cingulate, premotor, and calcarine cortices during the early recall phase, and activations associated with retrieving dangerous cues decreased in the occipital pole during the late recall phase. Additionally, correlations between decreased activation and elevated posttraumatic stress symptoms were observed. Conclusion: These findings suggest that activations associated with processing low arousal contextual information, safety cues, and extinguished fear cues decreased during the pandemic. These changes in brain activation may have contributed to the increase in mental health disturbances observed during this time.
ABSTRACT
Posttraumatic stress symptoms (PTSS) develop as sequelae from traumatic injuries. Limited studies suggest that using opioids to reduce acute pain immediately after trauma may also reduce subsequent PTSS, but other pain medications rarely have been examined for preventing acute PTSS. The current study examined the effects of commonly used pain medications, opioid and nonsteroidal anti-inflammatory drugs (NSAIDs), on PTSS after acute traumatic injuries. Participants ( n = 71) were categorized into opioid or NSAID group according to their medical records and self-reported medication use. Their PTSS were assessed using posttraumatic stress disorder checklist twice within 2 weeks after trauma. Participants' pain levels reduced from pretreatment to follow-up in both groups, F (1, 55) = 6.696, P = 0.012, partial η 2 = 0.109. Interestingly, a significant interaction between time and medication group on PTSS reached statistical significance, F (1, 69) = 6.014, P = 0.017, partial η 2 = 0.080. Follow-up analyses revealed that this interaction was driven by a significant PTSS reduction only in opioid but not in NSAID group. These findings suggested that pain reduction alone is not sufficient to reduce acute PTSS in the NSAID group, highlighting the need to continue further investigations into the mechanisms by which opioids reduce PTSS in the early posttrauma period.
