Title: The impact of COVID-19 pandemic-related disruptions on neuroinflammation in chronic pain patients.
Presenter: Ludovica Brusaferri, PhD, postdoc, Harvard Medical School, US
Methodology, findings and conclusions of the research
While COVID-19 research has seen an explosion in the literature, the impact of pandemic-related societal and lifestyle disruptions on brain health among the uninfected remains under-explored. Since pandemic onset, an increased prevalence of fatigue, dyscognition (i.e., “brain fog”) and other symptoms have been reported, including among the non-infected, and results from both clinical and preclinical literature raise the possibility that (neuro)inflammation might be a potential mechanism underlying those symptoms. In our last study, we showed that non-infected healthy volunteers examined after the onset of the COVID-19 pandemic exhibited higher levels of multiple (neuro)inflammation markers with respect to those examined before. Here we extended our investigation to patients with chronic pain conditions, specifically chronic low back pain (cLBP) and migraine (MIG), both of which are conditions previously linked to neuroinflammation in the pre-COVID era.
Ninety-seven subjects from both pain populations underwent PET/MRI imaging with the TSPO ligand [11C]PBR28; this protein is unregulated during neuroinflammatory states, serving as a suitable diagnostic biomarker for neuroinflammation. [11C]PBR28 signal was compared across Pandemic and Pre-Pandemic groups in voxel-wise analyses; sub-analyses were also conducted to rule out possible confounding factors, such as unbalanced demographics and history of COVID-19 infection. Participants from the Pandemic cohort showed increased [11C]PBR28 uptake in both groups overlapping within a cluster encompassing the anterior cingulate cortex (aCC), amygdala, insular cortex (IC) and frontal orbital cortex (FOC), supporting the hypothesis that the pandemic-related societal/lifestyle disruptions may have been accompanied by increased neuroinflammation. A negative correlation was also observed between TSPO metrics and pain clinical variables (migraine frequency for the MIG group), suggesting that TSPO elevations may reflect anti-inflammatory/protective mechanisms. This study lays the foundation to understand the mutual interaction between pandemic-related disruptions (not related to COVID-19 infection) and pre-existing neuroinflammatory conditions, including migraine.
Implications of the research for understanding migraine and/or its comorbidities
This study has implications for understanding mutual interactions between social stressors and pain, possible early progression of pre-existent neuroinflammatory diseases, impacts on immune tolerance and possible changes in the baseline of ongoing and/or future clinical trials during the COVID-19 pandemic.