Cluster headache

Abstract

Unlike migraine, cluster headache is less common, 4-6 times more common in men and in blacks. The etiology is unknown. About 70% of patients are smokers, and it has been suggested that chronic irritation of the ganglion by cigarette smoke may cause unilateral hyperreactivity. The hypocretin 2 receptor gene (HERTR2) has been suggested to modulate the risk of disease. The pathophysiology is related to the activation of the trigeminovascular system. The circadian rhythmicity of headache is associated with involvement of the suprachiasmatic nucleus and adaptive changes in hypothalamic functions.
Clinically, the onset of the disease is later than in migraine, around 28 years of age. It proceeds with attacks of headache accompanied by autonomic symptoms. Prodromal symptoms precede the headache attack. They include lethargy, mood swings (depression, apathy, anxiety, euphoria or hypomanic behavior), followed after a few minutes by neurological symptoms such as disorientation, drowsiness and yawning, irritability, paresthesias and strange body sensations. An attack of headache begins suddenly and rapidly with moderate, always unilateral pain in and around the eye (retroorbital) or in the temporal region, followed by nasal congestion. The attack lasts between 15 minutes and 3 hours, most often from 30 minutes to 2 hours. The pain is always unbearably strong, being weaker at the beginning and end of the attack.
During the day the attacks tend to occur at the same time, characteristic of the patient, like clockwork. Most often this occurs between 1 and 2 o'clock at night, and during the day between 1 and 3 o'clock, or about 9 o'clock. The frequency of attacks is very individual and varies from one during the day to 8 (average 4) daily. Local cranial autonomic symptoms develop on the ipsilateral side of the headache. They include lacrimation (in 90%), conjunctival inection (84%), nasal congestion (75%), and rhinorrhea (72%). Partial Horner's syndrome, with mild ipsilateral ptosis, miosis, and eyelid edema was seen in 69% of patients. Behavior in 93% of patients is very typical, they cannot continue their normal activity during the attack, do not stand still, do not lie down, do not seek help and do not tolerate the presence of other people. Attack treatment is conducted with 100% oxygen inhalation, corticosteroids, triptans, and intranasal lidocaine or cocaine. Prophylactic treatment is carried out during the period with calcium antagonists, corticosteroids, lithium carbonate or anticonvulsants.