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Updated: Feb 18, 2026

Targeted Neuronal Injury for the Non-Invasive Disconnection of Brain Circuitry

Targeted Neuronal Injury for the Non-Invasive Disconnection of Brain Circuitry

Published on: September 27, 2020

Spinal Cord Injury Disrupts Resting-State Networks in the Human Brain.

Ammar H Hawasli^1,2,3, Jerrel Rutlin⁴, Jarod L Roland¹

¹1 Department of Neurological Surgery, Washington University School of Medicine , Saint Louis, Missouri.

Journal of Neurotrauma

|November 29, 2017

Summary

This summary is machine-generated.

Spinal cord injury (SCI) significantly alters brain functional networks, impacting connectivity within key resting-state networks (RSNs). These changes, particularly in complete SCI, may predict recovery and guide future therapies for brain plasticity.

Keywords:

MRI SCI biomarkers neuroplasticity

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Published on: May 28, 2014

Area of Science:

Neuroscience
Neurology
Radiology

Background:

Spinal cord injury (SCI) affects over 253,000 individuals in the US, yet its impact on brain networks remains poorly understood.
Standard spinal MRI offers only structural data, lacking insights into functional brain connectivity.
Resting-state functional MRI (RS-fMRI) is crucial for quantifying network connectivity and detecting disease-related changes.

Purpose of the Study:

To investigate how spinal cord injury (SCI) affects brain functional connectivity using resting-state functional MRI (RS-fMRI).
To identify specific resting-state networks (RSNs) altered by SCI and explore differences between complete and incomplete injuries.
To examine temporal changes in brain network connectivity following SCI.

Main Methods:

Acquired blood oxygen-dependent RS-fMRI data from 10 SCI subjects and performed functional assessments.
Utilized seed-based correlation mapping to analyze five RSNs: default-mode (DMN), dorsal-attention (DAN), salience (SAL), control (CON), and somatomotor (SMN).
Compared RSNs between SCI patients and controls using false-discovery rate-corrected t tests, analyzing complete vs. incomplete SCI cohorts and temporal changes.

Main Results:

SCI reduced connectivity within the SAL, SMN, and DMN, and disrupted anti-correlated connectivity between CON and SMN.
Complete SCI, unlike incomplete SCI, disrupted connectivity within SAL, DAN, SMN, DMN, and between CON and SMN.
Over time, SCI led to decreased connectivity between the primary motor and somatosensory cortices, and between visual and sensorimotor cortices.

Conclusions:

SCI induces significant functional network plasticity in the brain.
Altered brain connectivity following SCI may serve as potential biomarkers for predicting functional recovery.
These findings can inform the development of targeted therapies for SCI rehabilitation.