Neuropathic Pain Induced by Spinal Cord Injury from the Glia Perspective and Its Treatment

Cellular and Molecular Neurobiology, 2024 · DOI: https://doi.org/10.1007/s10571-024-01517-x · Published: November 28, 2024

Spinal Cord Injury Neurology Pain Management

Simple Explanation

Neuropathic pain after spinal cord injury (SCI) is caused by glial cells, ectopic firing of neurons endings and their intra- and extracellular signaling mechanisms. Another mechanism is the release of substances by glia, which keeps the sensitivity of dorsal horn neurons even in regions distant from the site of injury. Here, we review, the models and identifications of SCI-induced neuropathic pain (SCI-NP), the mechanisms of SCI-NP related to glia, and the treatments of SCI-NP.

Study Duration

Not specified

Participants

Not specified

Evidence Level

Review Paper

Key Findings

1
Activated astrocytes and microglia are essential for the development and maintenance of SCI-NP.
2
Reactive astrocytes develop a glial scar, which restricts the growth of the injury and the regeneration of axons.
3
Microglia contribute to central sensitization following SCI by triggering the NLRP3 inflammasome.

Research Summary

Neuropathic pain after SCI is caused by glial cells, ectopic firing of neurons endings and their intra- and extracellular signaling mechanisms. SCI causes activation of astrocytes and microglia across the entire spinal dorsal horn, which has an important role in neuropathic pain. While there have been some advancements in detecting neuropathic pain that occurs after SCI and understanding the exact processes behind it, only a limited number of treatment methods targeting these specific mechanisms have been used in clinical practice.

Practical Implications

Targeted Therapies

Develop treatment modalities that target the mechanisms involved in SCI-NP, focusing on glial cells.

Personalized Medicine

Account for sex differences in SCI-NP to provide different therapy approaches.

Gene Therapy

Explore gene therapy to treat SCI-NP by blocking inflammatory activation of glial cells or associated gene expression.

Study Limitations

1
Clinicians have paid little attention to the causes of post-SCI chronic pain
2
SCI-NP is often challenging.
3
Neuropathic pain is acknowledged to be long-lasting and resistant to many of the current therapies available.

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