Evidence map›Paper›PMID 38311745›Full record

ReviewThe journal of headache and pain2024

Arterial hypertension in the chronic evolution of migraine: bystander or risk factor? An overview.

Federico Mazzacane, Gloria Vaghi, Matteo Cotta Ramusino, Giulia Perini, Alfredo Costa

Open access · goldAbstract readReview
In one paragraph

Review in The journal of headache and pain, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. 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

5 authors at 2 institutions in 1 country.

Federico MazzacaneDepartment of Brain and Behavioral Sciences, University of Pavia, 27100, Pavia, Italy.
Gloria VaghiDepartment of Brain and Behavioral Sciences, University of Pavia, 27100, Pavia, Italy. gloria.vaghi01@universitadipavia.it.
Matteo Cotta RamusinoUnit of Behavioral Neurology, IRCCS Mondino Foundation, Via Mondino 2, 27100, Pavia, Italy.
Giulia PeriniUnit of Behavioral Neurology, IRCCS Mondino Foundation, Via Mondino 2, 27100, Pavia, Italy.
Alfredo CostaDepartment of Brain and Behavioral Sciences, University of Pavia, 27100, Pavia, Italy.
Fondazione Istituto Neurologico Nazionale Casimiro Mondino · ITUniversity of Pavia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSeveral risk factors are associated with the chronic evolution of migraine. Clinical and preclinical studies have provided data about the role of hypertension (HT) as one of the potential modifiable risk factors of chronic migraine (CM). This review is focused on the biological and clinical evidence supporting common mechanisms underlying HT and migraine and the potential role of HT in the transition from episodic to chronic migraine.

methodsWe conducted a narrative review from a literature search covering the available evidence from studies investigating: i) the role of HT in the transition to CM in clinical practice; ii) the biological mechanisms potentially underpinning the association between HT and evolution to CM; iii) the role of antihypertensive medications in migraine prophylaxis.

resultsHT proved to be at the base of multiple mechanisms underlying migraine and migraine chronicization. Endothelial dysfunction, blood-brain barrier alterations, calcitonin gene-related peptide signaling, and renin-angiotensin-aldosterone system dysregulation are involved in the worsening effect of HT on migraine frequency, and the role of HT in the transition to CM is supported by clinical observations.

conclusionsThe observed evidence supports HT contribution to CM evolution due to shared pathophysiologic mechanisms. While a bidirectional influence appears to be ascertained, data are still lacking about the one-way role of HT as direct risk factor for CM transition. Further research is needed to confirm a causal role of HT in this process.

Indexed as

HypertensionMigraine DisordersCalcitonin Gene-Related PeptideHumansRenin-Angiotensin SystemRisk FactorsCalcitonin Gene-Related PeptideArterial hypertensionChronicizationChronic migraineEndothelial dysfunctionMigraine

Identifiers

PMID38311745
PMCPMC10840219
OpenAlexW4392735605

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.