Cluster Headache

Core clinical features

Cluster attacks cause excruciating unilateral orbital, supraorbital or temporal pain lasting about 15–180 minutes when untreated, often described as burning, stabbing or boring. Attacks typically occur from once every other day up to 8 per day in “clusters” over weeks to months, separated by remission periods that can last months to years.​

Autonomic signs and behavior

Pain is accompanied by ipsilateral autonomic features such as conjunctival injection and tearing, nasal congestion or rhinorrhea, eyelid edema, forehead/facial sweating, miosis and/or ptosis. Patients are usually agitated and restless during attacks, often pacing or rocking, in contrast to migraine where patients prefer to lie still.​

Episodic vs chronic forms

Episodic cluster headache involves bouts lasting 7 days to 1 year separated by pain‑free periods of at least 3 months. Chronic cluster headache is defined by attacks for more than 1 year without remission or with remissions lasting less than 3 months, affecting roughly 10–20% of patients.​

Triggers and pathophysiology

Attacks often show circadian and circannual patterns, frequently occurring at the same clock time each day and clustering in particular seasons, implicating hypothalamic dysfunction in a trigeminal autonomic cephalgia framework. Alcohol during a cluster period, vasodilators such as nitroglycerin, and changes in sleep pattern can precipitate attacks, whereas these triggers may not provoke pain outside active cluster bouts.​

Acute and preventive treatment

Evidence‑based acute therapies include high‑flow 100% oxygen via non‑rebreather mask, subcutaneous or intranasal triptans (e.g., sumatriptan, zolmitriptan), and sometimes intranasal lidocaine. Preventive strategies center on verapamil (often at higher doses with ECG monitoring), with adjuncts such as short steroid tapers for transitional therapy, lithium, topiramate, CGRP‑pathway agents in some jurisdictions, and, in refractory cases, neuromodulation approaches (e.g., occipital nerve or sphenopalatine ganglion stimulation).​

Key Ocular Signs

Common manifestations include conjunctival injection (redness) and lacrimation (tearing) on the affected side, occurring in over 90% of attacks. Ptosis (drooping eyelid) and eyelid edema (swelling) affect about 50-80% of patients, while miosis (smaller pupil) is seen in roughly 30-50%.