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Chronic Post-Ischemia Pain Model for Complex Regional Pain Syndrome Type-I in Rats

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Epigenomic Interactions Between Chronic Pain and Recurrent Pressure Injuries After Spinal Cord Injury.

Letitia Y Graves^1,2, Melissa R Alcorn¹, E Ricky Chan³

¹VA Northeast Ohio Healthcare System, Cleveland, OH 44106, USA.

|August 22, 2025

Summary

DNA methylation patterns in spinal cord injury (SCI) individuals reveal links to chronic pain and recurrent pressure injuries (PrI). Specific methylation sites and gene regions are associated with these conditions, suggesting a complex regulatory network.

Keywords:

DNA methylation chronic pain neuropathic pain recurrent pressure injury secondary health condition spinal cord injury

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Published on: April 11, 2018

Area of Science:

Epigenetics
Neuroscience
Genomics

Background:

Spinal cord injury (SCI) survivors often experience chronic pain and pressure injuries (PrI).
Understanding the biological underpinnings of these comorbidities is crucial for developing targeted interventions.
DNA methylation, an epigenetic mechanism, may play a role in the pathophysiology of SCI complications.

Purpose of the Study:

To investigate DNA methylation variations associated with chronic pain.
To examine DNA methylation patterns linked to the propensity for recurrent pressure injuries (PrI) in individuals with SCI.
To explore whether DNA methylation mediates the co-occurrence of chronic pain and recurrent PrI.

Main Methods:

Whole blood DNA methylation was quantified using Illumina genome-wide arrays (EPIC and EPICv2) in 81 individuals with SCI.
Clinical data, including chronic pain status and recurrent PrI history, were collected.
Differential methylation analysis was performed using R packages limma, DMRcate, and mCSEA.

Main Results:

Three differentially methylated positions (DMPs) and a region in the BLCAP/NNAT locus were associated with chronic pain in the SCI cohort.
In individuals without recurrent PrI, the same sites were linked to pain; however, two novel hypermethylated sites and a region in FDFT1 were identified in those with recurrent PrI.
Gene enrichment analysis revealed shared disorders and ontology terms between chronic pain and recurrent PrI phenotypes.

Conclusions:

Differential methylation analysis identified shared genes and regulatory regions associated with chronic pain and PrI history in SCI.
These findings suggest a broader gene regulatory network underlying chronic pain and recurrent PrI in SCI.
Further validation of these epigenetic associations is warranted.