Evidence map›Paper›PMID 25017893›Full record

ReviewExperimental neurology2014

The paradox of chronic neuroinflammation, systemic immune suppression, autoimmunity after traumatic chronic spinal cord injury.

Jan M Schwab, Yi Zhang, Marcel A Kopp, Benedikt Brommer, Phillip G Popovich

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Experimental neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
146citing papers in PubMed, 3 pooled it
10.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

146 citing papers in PubMed, 3 syntheses or guidelines pooled it, 251 citations in OpenAlex.

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  13. Nanoparticle and epothilone D combinatorial intervention improves motor performance and regeneration in chronic cervical spinal cord injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
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86 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Jan M Schwab *Department of Neurology and Experimental Neurology, Clinical and Experimental Spinal Cord Injury Research (Neuroparaplegiology), Charite - Universitatsmedizin Berlin, D-10117 Berlin, Germany.
Yi Zhang *Center for Brain and Spinal Cord Repair, Department of Neuroscience, Wexner Medical Center, The Ohio State University Medical Center, Columbus, OH 43210, USA.
Marcel A KoppDepartment of Neurology and Experimental Neurology, Clinical and Experimental Spinal Cord Injury Research (Neuroparaplegiology), Charite - Universitatsmedizin Berlin, D-10117 Berlin, Germany.
Benedikt BrommerDepartment of Neurology and Experimental Neurology, Clinical and Experimental Spinal Cord Injury Research (Neuroparaplegiology), Charite - Universitatsmedizin Berlin, D-10117 Berlin, Germany.
Phillip G PopovichCenter for Brain and Spinal Cord Repair, Department of Neuroscience, Wexner Medical Center, The Ohio State University Medical Center, Columbus, OH 43210, USA.
Charité - Universitätsmedizin Berlin · DEThe Ohio State University Wexner Medical Center · US

Funding

T-cell Functions in the Injured Spinal CordR01NS047175 · NINDS · OHIO STATE UNIVERSITY · PI POPOVICH, PHILLIP G · 2003 to 2013
$3.3M
Autonomic dysreflexia and SCI immune suppressionR21NS067260 · NINDS · OHIO STATE UNIVERSITY · PI POPOVICH, PHILLIP G · 2009 to 2010
$417k
NINDS NIH HHS R01 NS047175NINDS NIH HHS R21 NS067260
6 · The paper itself

Abstract

During the transition from acute to chronic stages of recovery after spinal cord injury (SCI), there is an evolving state of immunologic dysfunction that exacerbates the problems associated with the more clinically obvious neurologic deficits. Since injury directly affects cells embedded within the "immune privileged/specialized" milieu of the spinal cord, maladaptive or inefficient responses are likely to occur. Collectively, these responses qualify as part of the continuum of "SCI disease" and are important therapeutic targets to improve neural repair and neurological outcome. Generic immune suppressive therapies have been largely unsuccessful, mostly because inflammation and immunity exert both beneficial (plasticity enhancing) and detrimental (e.g. glia- and neurodegenerative; secondary damage) effects and these functions change over time. Moreover, "compartimentalized" investigations, limited to only intraspinal inflammation and associated cellular or molecular changes in the spinal cord, neglect the reality that the structure and function of the CNS are influenced by systemic immune challenges and that the immune system is 'hardwired' into the nervous system. Here, we consider this interplay during the progression from acute to chronic SCI. Specifically, we survey impaired/non-resolving intraspinal inflammation and the paradox of systemic inflammatory responses in the context of ongoing chronic immune suppression and autoimmunity. The concepts of systemic inflammatory response syndrome (SIRS), compensatory anti-inflammatory response syndrome (CARS) and "neurogenic" spinal cord injury-induced immune depression syndrome (SCI-IDS) are discussed as determinants of impaired "host-defense" and trauma-induced autoimmunity.

Indexed as

AnimalsAutoimmunityChronic DiseaseHumansImmune ToleranceInflammationInflammation MediatorsSpinal Cord InjuriesInflammation MediatorsAdaptive immune responseAutoimmunityInnate immune responseSpinal cord injury

Identifiers

PMID25017893
PMCPMC4099970
OpenAlexW1991275594

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.