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Interictal and postictal contingent negative variation in migraine without aura
E J Mulder1, W H Linssen, J Passchier
1Department of Biological Psychology, Vrije Universiteit, De Boelelaan 1111, 1081 HV, Amsterdam, The Netherlands.
Headache
|February 13, 2001
Summary
Migraine without aura patients did not show enhanced cortical hyperexcitability between attacks. Sumatriptan use after an attack, however, led to reduced contingent negative variation (CNV) amplitudes, suggesting temporary cortical hypoexcitability.
Area of Science:
- Neuroscience
- Clinical Neurology
Background:
- Cortical hyperexcitability is hypothesized to underlie enhanced contingent negative variation (CNV) amplitudes and impaired habituation in migraine without aura during interictal periods.
- These neurophysiological markers reportedly normalize during migraine attacks.
Purpose of the Study:
- To replicate interictal findings of cortical hyperexcitability in migraine without aura.
- To investigate CNV amplitudes during the postattack period following both sumatriptan and habitual non-vasoactive medication treatments.
Main Methods:
- A case-control study involving 12 patients with migraine without aura and matched healthy controls.
- Contingent negative variation (CNV) recordings were performed during interictal, postattack (sumatriptan-treated), and postattack (habitual medication-treated) periods.
Main Results:
- The study did not confirm enhanced CNV amplitudes or impaired habituation in the interictal period for migraine without aura patients.
- A significant decrease in CNV early and late wave amplitudes was observed postattack, specifically after sumatriptan treatment.
- This reduction in CNV amplitudes, particularly over the frontal cortex, suggests potential cortical hypoexcitability.
Conclusions:
- The findings do not support the theory of interictal cortical hyperexcitability in migraine without aura.
- Sumatriptan administration postattack may induce transient cortical hypoexcitability, possibly by modulating central catecholaminergic pathways.