CLUSTER HEADACHE- SUICIDE HEADACHE: PATHOGENESIS, DIAGNOSIS, AND MANAGEMENT
Keywords:
Cluster headache, trigemino-autonomic cephalalgia, hypothalamusAbstract
Cluster headache is a primary headache disorder characterized by recurrent, strictly unilateral attacks of severe orbital or temporal pain, accompanied by ipsilateral cranial autonomic symptoms. Despite being clinically well defined for more than two centuries, its pathophysiology remains incompletely understood. Recent advances implicate trigeminovascular activation and hypothalamic dysfunction, particularly disturbances in circadian rhythm regulation, as central mechanisms. Functional imaging consistently demonstrates hypothalamic activation during cluster attacks and in related trigemino-autonomic cephalalgias, supporting a shared neurobiological basis. Diagnosis is clinical, guided by International Classification of Headache Disorders (ICHD) criteria, although neuroimaging may be warranted to exclude secondary causes. Acute management relies on subcutaneous sumatriptan and high-flow oxygen, with intranasal lidocaine and dihydroergotamine as adjuncts. Preventive therapy is essential to reduce attack frequency; verapamil remains the cornerstone, with lithium, corticosteroids, methysergide, and calcium channel blockers as additional options. Overall, evidence highlights the hypothalamus as a pivotal structure in cluster headache pathogenesis and a potential target for future therapies.
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