![]() The pathophysiology of migraine is much more complex. Several case series have found that pain in the periauricular and neck regions is of particularly high incidence and severity in cluster headache. ![]() Myalgia, localized tenderness, and local hematoma formation is common in cluster headache attacks and is most likely due to local cranial nerve (such as the trigeminal nerve, for example) and vascular activation, rather than peripheral nerve compression. A recent study by Magalhães et al argues that the pathophysiology of chronic cluster headache should be reconsidered and that a subclinical combined mechanism may explain this condition. These etiological factors account for the pathophysiology of cluster headache – both the acute and, for the majority of patients, the chronic form. Experimental data suggest that in cluster headache, meningeal inflammation (possibly as a result of vessel inflammation in the cavernous sinus) activates the trigeminovascular system in a central and peripheral manner and may cause dural phlogosis as a result of the phlogogenic effects of proinflammatory cytokines. However, there is no evidence of increased carotid artery pulsatility in patients with chronic cluster headache. ![]() Peripheral abnormalities in cluster headache include increased thickness of the inferior turbinate mucosa, intermittent rhinorrhea, and increased carotid artery pulsatile flow.
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