Inflammation and its role in neuroprotection, axonal regeneration and functional recovery after spinal cord injury

Exp Neurol, 2008 · DOI: 10.1016/j.expneurol.2007.06.009 · Published: February 1, 2008

Simple Explanation

Trauma to the central nervous system (CNS) triggers inflammation and activation of the immune system, which can both worsen the damage and stimulate repair mechanisms. The role of neuroinflammation is controversial, with both beneficial and detrimental effects being attributed to various immune components. This review addresses the complexities of neuroinflammation after spinal cord injury (SCI) and discusses therapies that target neuroinflammatory cascades.

Study Duration

Not specified

Participants

Not specified

Evidence Level

Review

Key Findings

1
The inflammatory response in the brain differs from that in the spinal cord in terms of timing, composition, and magnitude.
2
Neuroinflammatory responses to SCI vary between species and strains, indicating a genetic influence on post-traumatic neuroinflammation.
3
Changes in blood-brain barrier permeability are a prelude to inflammation and are influenced by inflammatory mediators.

Research Summary

Inflammation following SCI has been shown to have both pathogenic and pivotal roles in tissue repair. A challenge for researchers is to learn how to control cross-talk between the nervous and immune systems to minimize delayed neurodegeneration while promoting axonal plasticity and regeneration. Greater appreciation is needed for how SCI influences leukocyte development, activation and mobilization within and from peripheral lymphoid tissues.

Practical Implications

Site-Specific Therapies

Understanding the differences between brain and spinal cord inflammation could lead to novel site-specific therapies.

Personalized Treatment

Acknowledging genetic variability in inflammatory responses suggests that treatments should be tailored to individual patients.

Controlled Vasoactive Properties

The vasoactive properties of neuroinflammation could be harnessed to deliver drugs to the chronically injured brain or spinal cord.

Study Limitations

1
Incomplete understanding of mechanisms controlling divergent immune functions.
2
Contradictory effects of lymphocytes on the injured CNS.
3
Questionable safety of expanding autoreactive lymphocytes for repair.

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