Mechanisms involved
This condition is explained through the mechanisms below. Each one is taught as ordinary physiology first.
Secondary / contributing
Immune cells involvedWho is actually in the tissue
The trigeminovascular system runs alongside immune tissue, and they talk to each other.
Selected cell
Mast cell
Tissue sentinel packed with histamine, tryptase and prostaglandin granules. When it degranulates it recruits and sensitizes nearby nerve endings.
Dural mast cells degranulate near trigeminal endings, releasing histamine and CGRP-adjacent mediators that sensitize them.
Schematic drawings, not micrographs. Immune findings here describe mechanism and association; none of them are diagnostic tests.
What it is
A neurological condition with attacks of moderate to severe head pain plus sensory sensitivity, nausea, and often a prodrome hours before pain begins. Between attacks, thresholds remain lower than average — which is why triggers matter and why prevention outperforms rescue.
How the mechanisms produce this
- Trigeminovascular activation and CGRP release drive the pain phase; central sensitization shows up as scalp allodynia mid-attack.
- The same filtering mechanism that governs sensory tolerance sets the threshold for an attack.
- Estrogen withdrawal in the late luteal phase is one of the most reliable triggers described.
- Autonomic features — nausea, pallor, lightheadedness — are part of the attack, not a separate problem.
What tends to help
- Treat early in the attack; delayed treatment works less well once allodynia appears.
- Preventive treatment once attacks exceed roughly four monthly days, including CGRP-targeted options.
- Address the modifiable threshold factors: sleep regularity, hydration, meal timing, medication-overuse.
- Track against the cycle before concluding a treatment failed.
Where the evidence is thin
Why thresholds differ so much between people, and why some respond only to specific drug classes, is not well explained.