ReviewNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2008
Peripheral mechanism of action of antimigraine prophylactic drugs.
Review in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Migrainous facial palsy (MFP): the introduction of a new concept of neurovascular conflict and its preliminary clinical evidence.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2020Article
- Polytherapy for migraine prophylaxis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Migraine is a visceral pain. According to current theories, activation of trigeminocervical nerve endings releases calcitonin gene-related peptide and substance P, inducing vasodilation and plasma protein extravasation, leading to 'neurogenic' inflammation. Activation of the trigeminovascular system is followed by sensitisation of trigeminocervical fibres, maintaining a condition of hypersensitivity to non-noxious stimuli that support persistent pain during migraine attack. Other neurotransmitters (nitric oxide, bradykinins, 5-HT, etc.) play a role in regulating this complex mechanism. In this brief review, we consider the effect of drugs that, acting on the different transmitters involving in pain perception, can stop or inhibit these pathogenetic mechanisms.
Indexed as
Identifiers
18545913What OpenQuestion holds
Registered trials
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.