2015
DOI: 10.1016/j.npep.2015.03.006
|View full text |Cite|
|
Sign up to set email alerts
|

Migraine and neuropeptides

Abstract: Migraine is a common disabling neurovascular primary headache disorder. The pathomechanism is not clear, but extensive preclinical and clinical studies are ongoing. The structural basis of the leading hypothesis is the trigeminovascular system, which includes the trigeminal ganglion, the meningeal vasculature, and the distinct nuclei of the brainstem, the thalamus and the somatosensory cortex.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

1
85
0
2

Year Published

2016
2016
2020
2020

Publication Types

Select...
8
1

Relationship

1
8

Authors

Journals

citations
Cited by 108 publications
(88 citation statements)
references
References 191 publications
(261 reference statements)
1
85
0
2
Order By: Relevance
“…At the same time, the reaction time of mice to cold or hot stimulation was decreased after the application of NTG, most obviously in 4 hr. The expression levels of two pain‐related peptides, CGRP and NPY , in serum were increased by NTG. While the mouse head discomforts, the pain threshold decrease and the elevation of CGRP and NPY levels in serum were all attenuated by the VP administration, suggesting that VP played a protective role against migraine‐caused neural damage in NTG‐injected mice.…”
Section: Discussionmentioning
confidence: 99%
“…At the same time, the reaction time of mice to cold or hot stimulation was decreased after the application of NTG, most obviously in 4 hr. The expression levels of two pain‐related peptides, CGRP and NPY , in serum were increased by NTG. While the mouse head discomforts, the pain threshold decrease and the elevation of CGRP and NPY levels in serum were all attenuated by the VP administration, suggesting that VP played a protective role against migraine‐caused neural damage in NTG‐injected mice.…”
Section: Discussionmentioning
confidence: 99%
“…Beta-blockers (metoprolol, propranolol), calcium channel blockers (flunarizine), antiepileptic drugs (valproic acid, topiramate) or antidepressants (amitriptyline, venlafaxine) are recommended for migraine prevention [19]. Lately Botulinum toxin A (BoNTA) has proven to be effective and it improves the quality of life in chronic migraine treatment [28][29][30][31]. An important disadvantage of BoNTA is its route of administration: intramuscular injection in the muscles of the face and neck [28,30].…”
Section: Migrainementioning
confidence: 99%
“…picture of an 'inflammatory state' [33,34]. Neurogenic inflammation is presumed to be an important factor in various neurological diseases: brain injury [35] , neuropathic pain [36], epilepsy [37,38] and primary headache diseases [39].…”
Section: Neurogenic Inflammationmentioning
confidence: 99%
“…For example, inadequate regulation of the autonomic nervous system (ANS) (Ebinger et al, 2006, Geraud and Donnet, 2013, Melek et al, 2007), derangement of serotonin metabolism (Dussor, 2014, Hoffmann and Goadsby, 2014, Vollbracht and Rapoport, 2014), insensitive reaction to reduced oxygen in the vasculature and tissue (Friberg et al, 1994, Lacombe et al, 1992, Raddant and Russo, 2014), disruption of the normal pain pathways (Kroger and May, 2015), peculiar platelet metabolism (Danese et al, 2014, Gawel and Rose, 1982, Hanington, 1989), neurogenic inflammation (Tajti et al, 2015) and etc. (Alstadhaug, 2014).…”
Section: Introductionmentioning
confidence: 99%