Brain Structural Differences in Adults Reporting Localized Chronic Pains Mediate Risk for Suicidal Behaviors

Abstract

Background: Chronic pain is a global health priority. Mapping pain occurring at different body sites, and variability in brain circuitry related to widespread chronic pain, can elucidate nuanced roles of the central nervous system underlying chronic pain conditions. Chronic pain triples suicide risk; however, whether brain circuitry can inform this risk relationship has not been investigated. Methods: 11,298 participants (mean age: 64 years (range: 58-70), 55% female) with brain MRI from the UK Biobank with pain for more than 3 months in the head, neck/shoulders, back, abdomen, or hips and knees, were age-and-sex-matched to 11,298 pain-free controls. Regression models assessed cortical and subcortical structure differences between individuals reporting chronic pain and those without; mediation models determined the relationship between pain, brain structure and history of attempted suicide. Outcomes: Chronic pain, regardless of site was associated with, lower surface area throughout the cortex, lower volume in the brainstem, ventral diencephalon, cerebellum, and pallidum, lower cortical thickness in the anterior insula, and greater cortical thickness in the superior parietal cortex. When differentiated by pain site, participants with chronic headaches distinctly showed an overall thicker cortex compared with controls. Chronic pain was associated with an elevated risk for suicide attempt and this relationship was mediated by lower cerebellum volume. Interpretation: There are shared cortical mechanisms underlying chronic pain across body sites. An extensive thicker cortex in chronic headache was consistent with previous research. Cerebellum volume mediates the relationship between chronic pain and suicide attempt, serving as a potential biomarker prognostic for suicidal behaviors in chronic pain patients. Funding: National Science Foundation, National Institutes of Health

Competing Interest Statement

Conflict of Interest: NJ and PT were MPI of a grant from Biogen, Inc., for work unrelated to the contents of this manuscript. AG is a scientific consultant for Yamaha on works unrelated to the contents of this manuscript. EAM is a member of the scientific advisory boards of Danone, Axial Therapeutics, Amare, Mahana Therapeutics, Pendulum, Bloom Biosciences, and APC Microbiome Ireland.

Funding Statement

This study was supported by NIH grants R01 MH117601 (Jahanshad), R01 AG059874 (Jahanshad), P50 DK064539 (Mayer), U01 DK082370 (Mayer), R01 MD015904 (AG), R03 DK121025 (AG), NSF GRFP 2020290241 (Bhatt), UK Biobank Resource Application 11559.

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The individual-level MRI and phenotype UK Biobank data are available upon application to UK Biobank (https://www.ukbiobank.ac.uk/register-apply/). Data were accessed under UK Biobank Resource Application 11559.

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