Evidence map›Paper›PMID 39901107›Full record

ReviewThe journal of headache and pain2025

The link between spreading depolarization and innate immunity in the central nervous system.

Kadir Oguzhan Soylu, Muge Yemisci, Hulya Karatas

Abstract readReview
In one paragraph

Review in The journal of headache and pain, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
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

3 authors.

Kadir Oguzhan SoyluInstitute of Neurological Sciences and Psychiatry, Hacettepe University, Ankara, Türkiye.ORCID http://orcid.org/0000-0002-6286-6729
Muge YemisciInstitute of Neurological Sciences and Psychiatry, Faculty of Medicine, Department of Neurology, Hacettepe University, Neuroscience and Neurotechnology Center of Excellence (NÖROM), Ankara, Türkiye.ORCID http://orcid.org/0000-0002-1528-1998
Hulya KaratasInstitute of Neurological Sciences and Psychiatry, Hacettepe University, Neuroscience and Neurotechnology Center of Excellence (NÖROM), Ankara, Türkiye. karataskursun@gmail.com.ORCID http://orcid.org/0000-0003-4838-6320

Funding

Hacettepe Üniversitesi TSA-2022-19749
6 · The paper itself

Abstract

Spreading depolarization (SD) is a complex event that induces significant cellular stress in the central nervous system, leading to a robust inflammatory response without causing cell death in healthy tissues which may be called as neuro-parainflammation. Research has established a clear link between SD and the activation of pro-inflammatory pathways, particularly through the release of cytokines like interleukin-1β and tumor necrosis factor-α, and the involvement of inflammatory mediators such as cyclooxygenase-2 and high mobility group box 1 (HMGB1). Mechanistically, the opening of pannexin-1 (Panx1) channels and the activation of the (NOD)-like receptor family pyrin domain containing 3 (NLRP3) inflammasome play critical roles in this process, facilitating the release of inflammatory signals that can exacerbate conditions like migraine. Furthermore, the interplay between neurons and glial cells, particularly astrocytes and microglia, underscores the intricate nature of neuroinflammation triggered by SD. Importantly, these findings indicate that these inflammatory processes may also have systemic implications, affecting immune responses beyond the central nervous system. Overall, this body of work highlights the need for further exploration of the mechanisms underlying SD-induced inflammation and potential therapeutic targets to mitigate neuroinflammatory disorders. Inflammation extends beyond the central nervous system to peripheral structures, including the meninges and trigeminovascular system, which are critical for headache initiation. Genetic factors, particularly familial hemiplegic migraine (FHM), exacerbate neuroinflammatory responses to SD, leading to increased susceptibility and prolonged headache behaviors. Collectively, these findings underscore the complex cellular interactions and innate inflammatory processes underlying SD and their relevance to migraine mechanisms, suggesting potential avenues for therapeutic intervention.

Indexed as

Central Nervous SystemCortical Spreading DepressionImmunity, InnateMigraine DisordersNeuroinflammatory DiseasesAnimalsHumansCentral nervous systemInnate immunityMigraineNeuroinflammationSD

Identifiers

PMID39901107
PMCPMC11792447

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.