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The pathophysiology of migraine
Annals of the Academy of Medicine, Singapore
|January 1, 1985
Summary
A new neurogenic hypothesis suggests migraine originates from brainstem pathways, not humoral factors. Instability in these monoaminergic pathways may explain migraine symptoms and lead to better treatments.
Area of Science:
- Neuroscience
- Pharmacology
- Vascular Biology
Background:
- The humoral theory of migraine is being replaced by a neurogenic hypothesis.
- Intrinsic serotonergic and noradrenergic pathways connect the brainstem to the cerebral cortex and spinal cord.
Purpose of the Study:
- To explore the neurogenic hypothesis of migraine.
- To explain migraine phenomena through central monoaminergic pathway instability.
Main Methods:
- Stimulation of the locus ceruleus in monkeys to observe effects on cerebral blood flow.
- Investigating the trigeminovascular reflex in cats and humans.
Main Results:
- Locus ceruleus stimulation affects cerebral vascular resistance and carotid arterial flow.
- Trigeminal nerve stimulation causes external carotid artery vasodilation.
- Vascular changes observed align with classical migraine patterns.
Conclusions:
- Excessive discharge of ascending monoaminergic pathways may initiate migraine.
- Monoamine depletion could activate pain pathways, leading to headache.
- Migraine pathophysiology may involve instability in central monoaminergic pathways, guiding future pharmacological interventions.