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The blood-brain barrier in migraine treatment.

Edvinsson, Lars LU and Tfelt-Hansen, P (2008) In Cephalalgia 28. p.1245-1258
Abstract
Salient aspects of the anatomy and function of the blood-barrier barrier (BBB) are reviewed in relation to migraine pathophysiology and treatment. The main function of the BBB is to limit the access of circulating substances to the neuropile. Smaller lipophilic substances have some access to the central nervous system by diffusion, whereas other substances can cross the BBB by carrier-mediated influx transport, receptor-mediated transcytosis and absorptive-mediated transcytosis. Studies of drugs relevant to migraine pathophysiology and treatment have been examined with the pressurized arteriography method. The drugs, given both luminally and abluminally, provide important notions regarding antimigraine site of action, probably abluminal to... (More)
Salient aspects of the anatomy and function of the blood-barrier barrier (BBB) are reviewed in relation to migraine pathophysiology and treatment. The main function of the BBB is to limit the access of circulating substances to the neuropile. Smaller lipophilic substances have some access to the central nervous system by diffusion, whereas other substances can cross the BBB by carrier-mediated influx transport, receptor-mediated transcytosis and absorptive-mediated transcytosis. Studies of drugs relevant to migraine pathophysiology and treatment have been examined with the pressurized arteriography method. The drugs, given both luminally and abluminally, provide important notions regarding antimigraine site of action, probably abluminal to the BBB. The problems with the BBB in animal models designed to study the pathophysiology, acute treatment models and preventive treatments are discussed with special emphasize on the triptans and calcitonin gene-related peptide (CGRP). The human experimental headache model, especially the use of glycerol trinitrate (the nitric oxide model), and experiences with CGRP administrations utilize the systemic administration of the agonists with effects on other vascular beds also. We discuss how this can be related to genuine migraine attacks. Our view is that there exists no clear proof of breakdown or leakage of the BBB during migraine attacks, and that antimigraine drugs need to pass the BBB for efficacy. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Cephalalgia
volume
28
pages
1245 - 1258
publisher
Wiley-Blackwell
external identifiers
  • wos:000261138600002
  • pmid:18727638
  • scopus:56549109172
ISSN
0333-1024
DOI
10.1111/j.1468-2982.2008.01675.x
language
English
LU publication?
yes
id
9a0b1136-f5f3-4d80-957b-65bff6137277 (old id 1222929)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/18727638?dopt=Abstract
date added to LUP
2008-09-03 12:40:06
date last changed
2017-05-14 04:27:34
@article{9a0b1136-f5f3-4d80-957b-65bff6137277,
  abstract     = {Salient aspects of the anatomy and function of the blood-barrier barrier (BBB) are reviewed in relation to migraine pathophysiology and treatment. The main function of the BBB is to limit the access of circulating substances to the neuropile. Smaller lipophilic substances have some access to the central nervous system by diffusion, whereas other substances can cross the BBB by carrier-mediated influx transport, receptor-mediated transcytosis and absorptive-mediated transcytosis. Studies of drugs relevant to migraine pathophysiology and treatment have been examined with the pressurized arteriography method. The drugs, given both luminally and abluminally, provide important notions regarding antimigraine site of action, probably abluminal to the BBB. The problems with the BBB in animal models designed to study the pathophysiology, acute treatment models and preventive treatments are discussed with special emphasize on the triptans and calcitonin gene-related peptide (CGRP). The human experimental headache model, especially the use of glycerol trinitrate (the nitric oxide model), and experiences with CGRP administrations utilize the systemic administration of the agonists with effects on other vascular beds also. We discuss how this can be related to genuine migraine attacks. Our view is that there exists no clear proof of breakdown or leakage of the BBB during migraine attacks, and that antimigraine drugs need to pass the BBB for efficacy.},
  author       = {Edvinsson, Lars and Tfelt-Hansen, P},
  issn         = {0333-1024},
  language     = {eng},
  pages        = {1245--1258},
  publisher    = {Wiley-Blackwell},
  series       = {Cephalalgia},
  title        = {The blood-brain barrier in migraine treatment.},
  url          = {http://dx.doi.org/10.1111/j.1468-2982.2008.01675.x},
  volume       = {28},
  year         = {2008},
}