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Vasoneuronal coupling in migraineurs after subcutaneous sumatriptan: a TCD study.
H Baezner1, W Steinke, M Daffertshofer
1Department of Neurology, University Heidelberg, Klinikum Mannheim, 68135, Mannheim, Germany. hansjoerb.baezner@zmf.ma.uni-heidelberg.de
Journal of the Neurological Sciences
|September 29, 1999
Summary
Sumatriptan, a migraine drug, does not appear to constrict cerebral arteries. This study found no evidence that sumatriptan causes secondary cerebral blood flow changes or increases the risk of cerebral ischemia.
Area of Science:
- Neuroscience
- Pharmacology
- Vascular Biology
Background:
- The trigeminovascular model explains migraine pain via neurogenic inflammation.
- Sumatriptan, a 5-HT1 agonist, targets meningeal artery vasoconstriction.
- Potential vasoconstrictive effects of sumatriptan on cerebral arteries remain unclear.
Purpose of the Study:
- To investigate sumatriptan's vasoactive effects on intracranial cerebral arteries.
- To assess potential changes in cerebral blood flow velocity (CBFV) and pulsatility index (PI) after sumatriptan administration.
- To evaluate the risk of cerebral ischemia associated with sumatriptan's cerebral circulation effects.
Main Methods:
- Studied 27 migraineurs measuring CBFV and PI in posterior cerebral arteries (PCAs).
- Monitored arterial blood pressure (BP), heart rate (HR), and respiration rate (RR).
- Assessed CBFV and PI changes before and 30 minutes after subcutaneous 6 mg sumatriptan, including response to visual stimulation.
Main Results:
- Despite a significant rise in diastolic blood pressure, mean CBFV remained constant.
- The relative increase in CBFV during visual stimulation did not change post-sumatriptan.
- No significant alterations in absolute mean CBFV or PI values were observed.
Conclusions:
- Sumatriptan does not appear to cause vasoconstriction in the human intracranial arterial circulation.
- The findings do not support the hypothesis that sumatriptan poses a risk of cerebral ischemia due to cerebral vasoconstriction.
- Sumatriptan's mechanism in migraine treatment likely does not involve significant cerebral arterial vasoactivity.