3.1 Diagnostic criteria:
A. At least 5 attacks fulfilling B–D
B. Severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting 15–180 min if untreated
C. Headache is accompanied by at least one of the following:
1. Ipsilateral conjunctival injection and/or lacrimation
2. Ipsilateral nasal congestion and/or rhinorrhoea
3. Forehead and facial sweating
4. Ipsilateral eyelid oedema
5. Ipsilateral forehead and facial sweating
6. Ipsilateral miosis and/or ptosis
7. A sense of restlessness or agitation
D. Attacks have a frequency from 1 every other day to 8/day
E. Not attributed to another disorder
3.1.1 Episodic cluster headache
Description: Occurs in periods lasting 7 days to 1 year separated by pain-free periods lasting 1 month or more
Diagnostic criteria:
A. All fulfilling criteria A–E of 3.1
B. At least 2 cluster periods lasting from 7 to 365 days and separated by pain-free remissions of ≥1 month
3.1.2 Chronic cluster headache
Description: Attacks occur for more than 1 year without remission or with remissions lasting less than 1 month
Diagnostic criteria:
A. All alphabetical headings of 3.1
B. Attacks recur over >1 year without remission periods or with remission periods <1 month
Core features of cluster headache are its periodicity, be it circadian or in terms of active and inactive bouts over weeks and months, and the lateralization of the pain. The typical cluster headache patient is male, with a 3:1 predominance, who has bouts of one to two attacks of relatively short duration unilateral pain every day for 8–10 weeks a year [4]. They are generally perfectly well between times. Patients with cluster headache tend to move about during attacks, pacing, rocking or even rubbing their head for relief. The pain is usually retro-orbital boring and very severe. It is associated with ipsilateral symptoms of cranial (parasympathetic) autonomic activation: a red or watering eye, the nose running or blocking, or cranial sympathetic dysfunction: eyelid droop. Cluster headache is likely to be a disorder involving neurons in or around the central pacemaker regions of the posterior hypothalamic grey matter [5, 6]. While cluster headache patients may also experience nausea, photophobia and phonophobia, the latter particularly photophobia tends to be ipsilateral to the pain in TACs [7].
10.3 Oxygen for Acute Cluster Headache
Treatment of acute cluster headache with 100 % oxygen was first suggested in the early 1950s [8]; interestingly it is not clear what the basis for the suggestion was [9]. Janks [10] set the use out very clearly as a sufferer himself, contributing the need for a rate of 10 L/min. Kudrow [11] reported the first series using 100 % oxygen at 7 L/min noting three-quarters of patients responded. He also reported oxygen to be better than sublingual ergotamine.
The scientific study of oxygen in cluster headache began with Fogan [12] who reported 19 patients in whom he compared air and oxygen, at 6 L/min, in a crossover study. Eleven patients completed the crossover. Oxygen was more effective than air.
The only substantial, well-powered study of oxygen in cluster headache used a double-blind, placebo (air)-controlled crossover design to treat four attacks in a balanced allocation. Oxygen 100 % at 12 L/min for 15 min rendered 78 % of patients pain free at 15 min while air rendered 20 % of patients pain free; the difference was highly significant with 78 subjects treating 298 attacks [13]. Oxygen reduced associated features and was extremely well tolerated. A proportion of patients have a rebound effect after the oxygen is stopped with the attacks returning; there is no large database to estimate this with although experience suggests it happens in up to one-third of patients. It can be responsible for a perception that attack frequency has been increased [14].
10.4 Triptans-Serotonin 5-HT1B/1D Receptor Agonists
Triptans were primarily developed by Humphrey and colleagues [18] for the acute treatment of migraine. The broad pharmacology of the triptans is similar [19], while there are some differences in pharmacokinetics and thus far only sumatriptan is available as an injection.
10.4.1 Sumatriptan by Injection
Sumatriptan 6 mg s/c was first shown to be effective in a randomized, double-blind, placebo-controlled crossover study in acute cluster headache where with a 10 % placebo response rate compared to a 46 % pain-free response for sumatriptan at 15 min. Thirteen per cent of the sumatriptan arm went on to use rescue oxygen while 49 % of the placebo arm rescued with oxygen [20]. In a dose-ranging study, sumatriptan 6 mg had a 75 % response rate at 15 min while 12 mg had a response rate of 80 % with overlapping confidence intervals [21]. Absent meaningful differences, the 6 mg was licensed. There is no attenuation of the effect even with very long bouts or in patients with chronic cluster headache [22, 23]. Sumatriptan 6 mg s/c is very fairly regarded as a gold-standard treatment of acute cluster headache [24].
10.4.2 Triptans – Intranasal
Sumatriptan 20 mg nasal spray was compared to placebo in a randomized placebo-controlled, two-attack crossover study. At 30 min, 47 % of patients using sumatriptan and 18 % using placebo were pain free, with a clear and significant benefit for active treatment [25]. While clearly not as effective in population terms as the injection, an important group of patients can derive benefit from the nasal spray. Having shown zolmitriptan 10 mg orally could be helpful in cluster headache [26], zolmitriptan 5 and 10 mg nasal spray were compared to placebo in two randomized double-blind, placebo-controlled three-attack crossover studies. In the European study, the pain-free rate at 30 min was 28 % for zolmitriptan 5 mg and 16 % for placebo [27]. In the US study, the pain-free rate at 15 min was 39 % for zolmitriptan 5 mg and 20 % for placebo [28]. Both the sumatriptan and zolmitriptan studies included patients with episodic and chronic cluster headache, as well as male and female patients, and neither of these variables predicted outcome. While slower in onset, and being useful for less number of patients, there are those who certainly find nasal sprays useful.
10.5 Dihydroergotamine
Parenteral dihydroergotamine (DHE) has been considered to be an effective abortive agent for cluster headaches for some time [8, 29]. There are no controlled trials of injectable DHE; however, clinical experience has demonstrated that intravenous administration can be helpful even when attacks have been resistant to other treatments [30]. DHE nasal spray 1 mg in a double-blind, placebo-controlled, crossover trial in 25 patients demonstrated a significant reduction in pain intensity in acute cluster headache [31]. The development of new, inhaled formulation thus far studied in migraine may be very useful and should certainly be tested in the cluster headache [32].
10.6 Lidocaine – Intranasal
Lidocaine (10 %) was reported to be effective at aborting nitroglycerin-induced cluster attacks in a double-blind, placebo-controlled study in nine patients [33]. Lidocaine or saline was applied for 5 min using a cotton swab in the area corresponding to the pterygopalatine fossa, under anterior rhinoscopy. The onset of effect was slow and the method not applicable to most patients. Based on this evidence, and our experience of a modest adjunctive effect, lidocaine solution 20–60 mg, given as nasal drops (4–6 % lidocaine solution) is prescribed, and applied bilaterally in the region of the pterygopalatine fossa. To ensure that the solution reaches the pterygopalatine foramen, the patient should be instructed to lie down horizontally as early as possible during an attack, with the head extending out of the bed, bent downwards 30–45° and rotated 20–30° towards the side of the headache. The tip of the dropper is inserted above the rostral end of the inferior turbinate and pushed inwards as deep as possible before dripping. The patient should be asked to maintain the position for about 2–5 min. It is certainly a cumbersome approach so that few patients find it useful in the medium term.
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