Evidence map›Paper›PMID 22328144›Full record

ReviewCurrent pain and headache reports2012

Endogenous mechanisms underlying the activation and sensitization of meningeal nociceptors: the role of immuno-vascular interactions and cortical spreading depression.

Dan Levy

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current pain and headache reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

67 citing papers in PubMed, 114 citations in OpenAlex.

  1. Trial
  2. Artificial intelligence analysis to explore synchronize exercise, cobalamin, and magnesium as new actors to therapeutic of migraine symptoms: a randomized, placebo-controlled trial.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022
    Trial
  3. Article
  4. Review
  5. Review
  6. Oxidative Stress and Migraine.Molecular neurobiology · 2024
    Review
  7. Review
  8. Review
  9. Review
  10. Immunological Profile of Vasospasm after Subarachnoid Hemorrhage.International journal of molecular sciences · 2023
    Review
  11. Review
  12. Lack of Association between CommonInternational journal of molecular sciences · 2023
    Article
  13. Article
  14. Review
  15. Review
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7 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

1 author at 1 institution in 1 country.

Dan LevyHeadache Research Laboratory, Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA. dlevy1@bidmc.harvard.edu
Beth Israel Deaconess Medical Center · US

Funding

MECHANISMS OF CSD-EVOKED PERSISTENT ACTIVATION OF MENINGEAL NOCICEPTORSR01NS078263 · NINDS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LEVY, DAN · 2013 to 2022
$3.1M
Peripheral Mechanisms of Posttraumatic HeadacheR01NS086830 · NINDS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LEVY, DAN · 2014 to 2018
$1.9M
Calvarial periosteal afferents in post-traumatic headacheR21NS077882 · NINDS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LEVY, DAN · 2011 to 2012
$479k
NINDS NIH HHS R01 NS078263NINDS NIH HHS R01 NS086830NINDS NIH HHS R21 NS077882
6 · The paper itself

Abstract

Migraine is considered one of the most prevalent neurological disorders but its underlying pathophysiology is poorly understood. Over the past two decades, it became widely accepted that activation of primary afferent nociceptive neurons that innervate the intracranial meninges serves as a key process that mediates the throbbing head pain of migraine. Knowledge about the endogenous factors that play a role in promoting this neural process during a migraine attack slowly begins to increase, and a better understanding remains one of the holy grails in migraine research. One endogenous process, which has been invoked as a major player in the genesis of migraine pain, is cortical spreading depression (CSD). Until recently, however, this notion was only supported by indirect evidence. Recently, electrophysiological data provided the first direct evidence that CSD is indeed a powerful endogenous process that can lead to persistent activation of meningeal nociceptors and the migraine pain pathway. CSD has been suggested to promote persistent sensitization and ensuing activation of meningeal nociceptors through a mechanism involving local neurogenic inflammation including the activation of mast cells and macrophages and subsequent release of inflammatory mediators. Local action of such nociceptive mediators can increase the responsiveness of meningeal nociceptors. Recent studies provided key experimental data implicating complex meningeal immuno-vascular interactions, in particular, the interplay between proinflammatory cytokines, the meningeal vasculature and immune cells, in enhancing the responses of meningeal nociceptors.

Indexed as

Cortical Spreading DepressionAnimalsCyclooxygenase 1Cyclooxygenase 2FemaleHumansInflammationMaleMeningesMigraine DisordersNociceptorsRatsReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IIRisk FactorsCyclooxygenase 1Cyclooxygenase 2PTGS1 protein, humanPTGS2 protein, humanReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type II

Identifiers

PMID22328144
OpenAlexW2045450157

What OpenQuestion holds

Textmetadata
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.