Abstract
Recently, we showed that healthy volunteers without a history of COVID-19 infection exhibited elevations in [11C]PBR28 PET signal, a measure of neuroinflammation, after the onset of the pandemic(Brusaferri et al., 2022). Here, we extended our investigations to two chronic pain populations, chronic low back pain (cLBP) and migraine (MIG), both conditions previously linked to neuroinflammation(Albrecht et al., 2019; Alshelh et al., 2021). Moreover, since a recent study documenteåd accelerated brain aging in young adults examined after pandemic onset(Gotlib et al., 2022), we tested the effects of the COVID-19 pandemic on brain age in chronic pain patients. 45 ‘Pre-Pandemic' patients (28 cLBP and 17 MIG) and 52 ‘Pandemic' patients (28 cLBP and 24 MIG), underwent [11C]PBR28 PET-MRI. [11C]PBR28 signal, and estimated brain age (Cole & Franke, 2017) were compared between Pre-Pandemic and Pandemic subgroups. Both Pandemic cLBP and MIG patients showed widespread increased [11C]PBR28 uptake, compared to the Pre-Pandemic patients, in regions including the anterior cingulate cortex, amygdala, insula and orbifronal cortex. Moreover, the estimated brain age of Pandemic-cLBP subjects was significantly higher than Pre-Pandemic cLBP(p=0.03). This result was not observed in the MIG cohort(p=0.42), and the correlation between PET signal and estimated brain age was not statistically significant in any region. This study supports the hypothesis that pandemic-related disruptions may be accompanied by increased neuroinflammation in chronic pain populations and, in cLBP patients, also by accelerated brain aging. While the specific mechanisms remain unknown, our results underscore the deleterious effect of the pandemic on chronic pain and brain health. P01-AT009965 nd R01-NS095937-01A1.