What is the current theory of pathophysiology in migraine headache?

The current theory of pathophysiology in migraine headache emphasizes the dysfunction of the trigeminovascular system. This system involves a complex interaction between the trigeminal nerve and the vascular structures in the brain. In migraines, this dysfunction can lead to the release of inflammatory mediators like CGRP (Calcitonin Gene-Related Peptide) and neuropeptides, which contribute to neurogenic inflammation and vasodilation of cerebral blood vessels.

This dysfunction is thought to trigger the cascade of events leading to the characteristic symptoms of migraine, such as headache, nausea, and sensitivity to light and sound. Understanding this mechanism is crucial for developing targeted treatments, including preventive and abortive therapies aimed at modulating this trigeminovascular response.

While issues like altered blood flow, increased intracranial pressure, or neurotransmitter imbalances can be associated with various headache disorders, they do not encapsulate the core pathophysiological changes specific to migraine headaches as effectively as the dysfunction of the trigeminovascular system.