Brain Functional Connectivity Correlates of Pain Catastrophizing in Post-traumatic Headache
Catherine Chong1, Simona Nikolova1, Gina Dumkrieger1, Michael Leonard2, Dani Smith2, Todd Schwedt1, Federico Bighiani3
1Mayo Clinic, 2Neurology, Mayo Clinic, 3Department of Brain and Behavioral Sciences, University of Pavia
Objective:
To investigate whether individuals’ pain experience, as measured by the Pain Catastrophizing Scale (PCS), is associated with magnetic resonance imaging resting-state functional connectivity (rs-FC) patterns in individuals with PTH.
Background:
Post-traumatic headache (PTH) is a common and debilitating sequela following mild traumatic brain injury (mTBI). Cognitive–affective factors, such as heightened attention or negative expectations about pain, have been linked to greater pain intensity and increased risk of pain persistence. Nevertheless, brain functional connectivity patterns associated with these cognitive-affective factors in PTH are poorly understood.
Design/Methods:
Rs-FC and PCS data were collected from 112 individuals with acute PTH (mean age: 40.5 ± 15.5; 75 females/ 37 males) within 1- 60 days post-mTBI. FC across 38 predefined regions-of-interest involved in pain, attention, and emotional processing was assessed using a seed-based correlation approach, controlling for age and sex. Correlations between FC and PCS total scores and subscores (rumination, helplessness, magnification) were investigated using linear regression corrected for multiple testing using Benjamini and Hochberg (FDR) with significance levels set as p < 0.05.
Results:
The mean PCS total score of the study population was 12.9 ± 10.6. Higher PCS scores were associated with hyperconnectivity between left amygdala and right cerebellum (raw p-value 0.0002; FDR p-value 0.0484; beta 0.0073). There were not significant associations between FC with PCS subscores.
Conclusions:
This finding suggests that cognitive-affective components of pain assessed using the PCS is associated with stronger FC among regions primarily involved in emotional (amygdala) and sensory–motor processing (cerebellum) in individuals with acute PTH. The identified strengthening of connectivity may amplify pain perception through heightened integration of affective and sensory signals. Overall, this study provides a novel insight into the neurobiological mechanisms contributing to maladaptive pain processing in individuals with PTH and suggests possible neural pathways involved in pain persistence.
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