# Explosive Synchronization of Brain Network Activity in Chronic Pain

> **NIH NIH R01** · UNIVERSITY OF MICHIGAN AT ANN ARBOR · 2022 · $720,375

## Abstract

PROJECT SUMMARY / ABSTRACT
Pain in the United States is common and costly, with over 1 in 3 individuals being afflicted causing an
economic burden approaching $600 billion annually. This problem results from our lack of understanding the
underlying mechanisms of most forms of chronic pain which in turn has hampered our ability to develop new
effective treatments. Fibromyalgia (FM) is a common chronic pain condition whose pathology is largely
unknown. Existing research suggests that the brain may play a significant role in pain expression in these
individuals. Although untested, an imbalance in excitatory and inhibitory brain activity may lead to an unstable
neural network sensitized to external stimuli and this may lead to pain in FM. Hypersensitive and unstable
networks have been observed in various physical and biological systems, and in such networks, small
perturbations can give rise to explosive and global propagation of activity over the system. One underlying
mechanism of hypersensitive systems, called explosive synchronization (ES), has been introduced and
actively studied over the past decade. ES is a phenomenon wherein small increases in stimulation strength
applied to a network, can lead to an abrupt state transition through global network synchronization. Here we
hypothesize that ES may be an underlying mechanism of the hypersensitivity of the FM brain, and a targeted
approach with non-invasive brain stimulation may reduce conditions or ES and subsequent pain in some of
these patients. Our pilot electroencephalogram (EEG) data showed that the FM brain displays network
configurations primed for ES. Individuals with more clinical pain had increased ES conditions within their brain
networks. Furthermore, when these same patients experienced an increase in pain following an experimental
pressure pain stimulus applied to the thumb, they exhibited a concomitant increase in ES. Understanding how
the development of hypersensitivity within the brain can lead to chronic pain is an unknown in the medical field
and is the major theme of this proposal. We posit that finding the underlying mechanism of hypersensitivity in
the FM brain could lead to a more fundamental understanding of the central nervous system sensitization seen
in this pain state (and potentially others), and targeting this phenomenon might be an effective new treatment
strategy. To achieve this goal, we propose three aims based on interdisciplinary approaches of neuroscience,
physics, medicine, and mathematics: Aim 1. Demonstrate that individuals with FM, as compared to pain free
controls, display brain characteristics of ES as assessed with EEG. Aim 2. Computationally model the
underlying mechanism(s) of the hypersensitive FM brain and identify key target regions that might reduce brain
hypersensitivity. Aim 3. Test the ability of high definition transcranial direct current stimulation (HD-tDCS) at
discrete network regions to reduce conditions of ES within the brain.

## Key facts

- **NIH application ID:** 10470381
- **Project number:** 5R01AT010060-04
- **Recipient organization:** UNIVERSITY OF MICHIGAN AT ANN ARBOR
- **Principal Investigator:** ALEXANDRE DASILVA
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $720,375
- **Award type:** 5
- **Project period:** 2019-09-10 → 2024-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10470381

## Citation

> US National Institutes of Health, RePORTER application 10470381, Explosive Synchronization of Brain Network Activity in Chronic Pain (5R01AT010060-04). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10470381. Licensed CC0.

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