Below is the abstract of an article published in the Annals of Neurology in 2016. This research studied the difference in genes that are responsible for inflammation in the tissue on the surface of the skull in individuals with nerve compression headache compared to individuals who did not have headache. The subjects with chronic headache had a significant increase in the genetic factors that cause inflammation, and a significant decrease in factors that reduce inflammation, leading to an overall inflammatory state on the outside of the head in people with chronic headache from nerve compression. This was the first study to show evidence of abnormality on the outside of the head in people with chronic headache. Link to article
Objective: Chronic migraine (CM) is often associated with chronic tenderness of pericranial muscles. A distinct increase in muscle tenderness prior to onset of occipital headache that eventually progresses into a full-blown migraine attack is common. This experience raises the possibility that some CM attacks originate outside the cranium. The objective of this study was to determine whether there are extracranial pathophysiologies in these headaches.
Methods: We biopsied and measured the expression of gene transcripts (mRNA) encoding proteins that play roles in immune and inflammatory responses in affected (ie, where the head hurts) calvarial periosteum of (1) patients whose CMs are associated with muscle tenderness and (2) patients with no history of headache.
Results: Expression of proinflammatory genes (eg, CCL8, TLR2) in the calvarial periosteum significantly increased in CM patients attesting to muscle tenderness, whereas expression of genes that suppress inflammation and immune cell differentiation (eg, IL10RA, CSF1R) decreased.
Interpretation: Because the upregulated genes were linked to activation of white blood cells, production of cytokines, and inhibition of NF-κB, and the downregulated genes were linked to prevention of macrophage activation and cell lysis, we suggest that the molecular environment surrounding periosteal pain fibers is inflamed and in turn activates trigeminovascular nociceptors that reach the affected periosteum through suture branches of intracranial meningeal nociceptors and/or somatic branches of the occipital nerve. This study provides the first set of evidence for localized extracranial pathophysiology in CM. Ann Neurol 2016;79:1000-1013.
© 2016 American Neurological Association.
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