Injury receptors at trigeminal nerve endings can stimulate the trigeminal nerve, thereby causing headache, activating the autonomic nervous system, and giving rise to symptoms such as nausea and vomiting.
The activation in the hypothalamus was seen solely in the pain state and was in the same area that was demonstrated to be activated in cluster headache patients [22] and patients suffering from paroxysmal hemicrania [90], suggesting considerable commonalities between SUNCT and cluster headache.
The first hypothesis was the convergence projection mechanism based on the fact that visceral afferent nerves from the heart and somatic afferent nerves from the head converged in the same spinal segments (C1 and C2 segments) belonging to TCC [26, 27]; when cardiac ischemic occurred, TCC was activated, leading to headache, similar to the reference pain of angina.
Several experiments showed that CSD could contribute to the headache via activating meningeal nociceptors [22, 23] and activating or disinhibiting the second-order neurons in the trigeminocervical complex (TCC) [22, 24, 25].
A "neurogenic inflammation" appears to be a key mechanism in causing the migraine headache by activating the trigeminal system [28].
It has been found that the pathways consisting of NO synthesis are activated in the experimental headache models such as nitroglycerin-induced headache [15].
Using the advanced method of voxel-based morphometry, it has been suggested that there is a correlation between the brain area activated specifically in acute cluster headache — the posterior hypothalamic grey matter — and an increase in grey matter in the same region.
Similar to inflammatory soup, AITC is a simple and direct method to activate the dural afferents responsible for headache pain.
Some foods can be a trigger for headache attacks, maybe because they activate biochemical mechanisms involved in headache disorder.
