Evidence map›Paper›PMID 18600349›Full record

ReviewSchmerz (Berlin, Germany)2008

[Pathophysiology of migraine and clinical implications].

M Schürks, H-C Diener

Abstract readEnglish AbstractReview
PubMed Publisher
In one paragraph

Review in Schmerz (Berlin, Germany), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. [What is migraine?].Der Nervenarzt · 2009
    Review
  3. Article
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

2 authors at 2 institutions in 2 countries.

M SchürksDivision of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 900 Commonwealth Avenue East, 3rd fl, Boston, MA 02215-1204, USA. mschuerks@rics.bwh.harvard.edu
H-C Diener
Harvard University · USKlinik und Poliklinik für Neurologie · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Migraine pathophysiology is determined by genetic and environmental factors. Based on altered cerebral habituation and low serotonin levels, certain triggers can elicit a migraine attack. Following initial unspecific prodromi, an aura follows in many patients which most often consists of visual symptoms. Cortical spreading depression is the electrophysiological correlate of the aura and can activate the trigemino-vascular system. This is one potential mechanism initiating the pain process. The characteristic unilateral pulsating headache is caused by a neurogenic inflammation in the meninges. Neck pain as reported by some patients is a migraine-specific feature, the anatomical basis being the trigemino-cervical complex. Functional changes in the pain processing system maintain the headache. Among these are sensitization of trigeminal nucleus caudalis neurons and an altered antinociception descending from the periaquaductal grey. Triptans have a peripheral and central mode of action, but they are no longer effective once central sensitization has occurred.

Indexed as

AnalgesicsBrainCortical Spreading DepressionCyclooxygenase 2 InhibitorsDihydroergotamineHumansMeningesMigraine DisordersMigraine with AuraNeural PathwaysNeuronal PlasticityNociceptorsRisk FactorsSerotoninSerotonin Receptor AgonistsSpinal Nerve RootsAnalgesicsCyclooxygenase 2 InhibitorsDihydroergotamineSerotoninSerotonin Receptor AgonistsTryptamines

Identifiers

PMID18600349
OpenAlexW1549033808

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.