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Background: Cluster headache, when compared with migraine or tension-type headache, is an uncommon form of primary neurovascular headache. However, with a prevalence of approximately 0.1% and a lengthy history of disabling and distressing episodic pain, cluster headache is an important neurologic problem. Methods: Patients (n ϭ 230) were recruited from our specialist clinic (24%) or from support groups (76%). All patients had a detailed history taken by at least two physicians and were assigned diagnoses according to the International Headache Society Diagnostic Guidelines. Results: The pain characteristics were of a strictly unilateral, predominantly retro-orbital (92%) and temporal pain (70%). Of the cranial autonomic features, lacrimation (91%) was the most common. Nausea (50%), photophobia (56%), and phonophobia (43%) often were noted, as was a sense of agitation or restlessness in 93% of patients. Typical migrainous aura was noted in 14% of this cohort. Most patients (79%) had episodic cluster headache, which was largely the same clinically as chronic cluster headache except for the persistence of attacks over time. The overall male-to-female ratio in this sample was 2.5:1, and this has decreased with time. Neither oral contraceptive use, menses, menopause, nor hormone replacement therapy had any consistent effect on cluster headache in women. Less than half of the patients had tried injectable sumatriptan, and many had not tried high-flow oxygen. Several unproven preventative agents that usually are used in migraine and an array of alternative therapies had been used; none of the latter was consistently effective. Conclusion: Patients with cluster headache offer a population of primary headache patients with devastating acute attacks of pain. The syndrome is stereotyped with effective evidence-based treatments that are prescribed in only half of patients having cluster headache.

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A 71‐year‐old woman presented with a short history of episodes of severe left‐sided orbital and temporal pain in paroxysms lasting 60 to 90 seconds, and accompanied by ipsilateral lacrimation of the eye, rhinorrhea, and conjunctival injection. Results of clinical examination and structural imaging were normal and a clinical diagnosis of SUNCT (short‐lasting unilateral neuralgiform pains with conjunctival injection and tearing) was made. The patient had a BOLD contrast–magnetic resonance imaging study in which significant activation was seen in the region of the ipsilateral hypothalamic gray, comparing the pain to pain‐free state. The region of activation was the same in this patient as has been reported in acute attacks of cluster headache.

Article abstract-Background: Cluster headache (CH), like migraine, is still regarded as a vascular headache although in both conditions a CNS cause has been suggested. Objective: To examine neurovascular mechanisms in CH. Methods: The authors used functional imaging with PET to investigate 18 CH patients (25 to 62 years old). Ten were in the active period (nine patients with induced attacks and one with spontaneous attack) and eight were out of their bout. In addition, the authors studied spontaneous CH and experimental pain in volunteers using MR angiography. Results: When an acute CH attack was triggered with nitroglycerin (NTG), activation occurred in the ipsilateral posterior inferior hypothalamic gray, the contralateral ventroposterior thalamus, the anterior cingulate cortex, the ipsilateral basal ganglia, the right anterior frontal lobe, and both insulae. In patients out of the bout who experienced only a mild NTG headache, activation was seen bilaterally in the insulae and frontal cortices, the anterior cingulate cortex, the right thalamus, and the left basal ganglia, but not in the hypothalamic gray area. In addition, the authors found a significant activation (vasodilatation) in the region of the major basal arteries that was caused in part by NTG but was also observed in the spontaneous case and could be induced by capsaicin injection into the forehead. Therefore, the vasodilatation is likely to be mediated by neural mechanisms involved in the acute CH attacks that are present in every human being. Conclusions: Dilatation of cranial vessels is not specific to any particular headache syndrome but generic to cranial neurovascular activation, probably mediated by the trigeminoparasympathetic reflex. These data confirm that CH is a CNS disorder best considered as a form of neurovascular headache.