Vasoneuronal coupling in migraineurs after subcutaneous sumatriptan: a TCDstudy

Citation
H. Baezner et al., Vasoneuronal coupling in migraineurs after subcutaneous sumatriptan: a TCDstudy, J NEUR SCI, 167(1), 1999, pp. 50-55
Citations number
38
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF THE NEUROLOGICAL SCIENCES
ISSN journal
0022510X → ACNP
Volume
167
Issue
1
Year of publication
1999
Pages
50 - 55
Database
ISI
SICI code
0022-510X(19990801)167:1<50:VCIMAS>2.0.ZU;2-R
Abstract
According to the trigeminovascular model of pain in migraine, sterile neuro genic inflammation of dural vessels stimulates nociceptive fibres of the tr igeminal nerve. Sumatriptan, a 5-HT1 receptor agonist, blocks this reaction and mediates vasoconstriction of meningeal arteries. However, it is uncert ain, whether sumatriptan also has a vasoconstrictive effect on cerebral art eries, which may influence vasoneuronal coupling and induce secondary cereb ral blood flow changes. We studied changes of cerebral blood flow velocity (CBFV) and the pulsatility index (PI) in the posterior cerebral artery (PCA ) after stimulus activation before, 10 min and 30 min after subcutaneous ap plication of 6 mg sumatriptan, in order to assess potential vasoactive effe cts on cerebral circulation. CBFV was recorded from both PCAs simultaneousl y in 27 migraineurs (twenty women, seven men, mean age 29 years), and arter ial blood pressure (BP), heart rate (HR) and respiration rate (RR) were mon itored. Although the mean diastolic blood pressure rose significantly from 75 mm Hg to 81 mm Hg (P<0.05) and systolic blood pressure and respiration r ates remained constant, average CBFV values remained constant. Similarly, t he relative increase of CBFV by visual stimulation, which is clearly higher compared to controls in other studies (55.0% before, 52.6% after 10 min, a nd 52.4% after 30 min), and absolute mean values for CBFV and PI did not ch ange after visual stimulation. These results provide evidence against the h ypothesis that sumatriptan produces vasoconstriction in the intracranial hu man arterial circulation as a potential risk of cerebral ischemia. (C) 1999 Elsevier Science B.V. All rights reserved.