Posted by jstone (199.174.228.49) on February 04, 2001 at 03:26:10:
In Reply to: Heat and CH posted by Frank on February 03, 2001 at 21:52:14:
A new cluster headache precipitant: increased body heat.(Research Letters)(Statistical Data Included)
Author/s: J N Blau
Issue: Sept 18, 1999
Exercise, a hot bath, or elevated environmental temperature provoked cluster headaches, within 1 h, in 75 out of 200 patients. This new observation accords with recognised precipitants--alcohol, histamine, and gyceryl trinitrate--perhaps via generalised vasodilatation or hypothalamic activation.
Characteristic autonomic disturbances during cluster headache attacks are conjunctival vasodilatation, lacrimation, miosis, ptosis, eyelid oedema, nasal congestion, forehead and facial sweating. These are generally accepted to be confined to the painful side of the face.(1) However, diffuse vasomotor symptoms, in particular feeling generally hot and bilateral perspiration of the head, neck and trunk, were mentioned by several patients, stimulating this study.
The diagnosis, based on a full history and physical examination, conformed to International Headache Society (IHS) criteria.(1) We personally took the history from 200 patients, during or soon after a cluster period, all with spontaneous attacks. 155 were male and 45 female, aged 19-72 (mean 41) years; 166 had episodic cluster headaches, 26 chronic cluster headaches, and eight alternated between the two conditions. All were specifically asked about altered body temperature, perspiration, and behaviour during attacks.
70 perspired bilaterally in face, neck, and body. Only seven sweated on the affected side of the face, but six felt hot bilaterally in the face without sweating. 28 perspired on both sides of the face and 23 just on the trunk; 66 did not experience increased body heat or perspiration. 72 stood in front of an open window, 56 walked outside the house, 79 applied cold to the affected eye or adjacent forehead or temple, but 18 applied heat to the painful region.
A new precipitant of cluster headache attacks emerged: increased body heat, either from the environment, a hot bath or central heating (n=52), generally within an hour, or from exertion (n=23), during or soon after exercise, including three during sexual intercourse (table). Two patients precipitated a new cluster period while on holiday in a hot climate. Alcohol, however, a well-recognised precipitant, was the most frequent trigger occurring in 118 patients in this series, the headache following 15-30 min after starting to drink.
The severe pain in one eye, increased tears, ipsilateral nasal blockage, and conjunctival vasodilatation, focus attention on the trigeminal area unilaterally. More widely distributed autonomic changes previously recorded include increased temperature and sweating on the nonaffected hemiface,(2) cardiac arrhythmias, raised blood pressure, nausea, vomiting, and diarrhoea.(3) Most authorities and IHS criteria maintain that sweating is confined to the affected hemiface. However, in this series only seven patients had unilateral facial perspiration.
Provocation by alcohol is readily recognised by patients, because attacks ensue 20-40 min after drinking. Experimentally, histamine and glyceryl trinitrate have been used to study attacks, although the delayed pain onset of 20-50 min remains unexplained. Precipitation by environmental heat or exercise, with close temporal relationship, reported here, conforms with the generalised vasodilatory effects of alcohol, histamine or glyceryl trinitrate. Sleep, during which most attacks occur, also causes diffuse vasodilatation. The therapeutic effect, via vasoconstriction, of ergot, the tryptan drugs, and oxygen inhalation is in keeping with these observations. Going out into the cold or applying cold to the affected hemiface seems a normal response to vasodilatation, but it is difficult to explain why some patients apply heat, unless it is as a form of counterirritation.
The underlying pathogenesis of cluster headaches remains undetermined, in spite of extensive investigation.(3) Provocation by sleep, alcohol, and by increased body heat raises the possibility that generalised vasodilatation is primary, stimulating or stimulated by the hypothalamus, and local symptoms and signs in and around the eye are a secondary manifestation. These generalised autonomic symptoms support hypothalamic activation,(4) rather than primary cavernous sinus origin.(5)
Detailed study of the preliminary phases of cluster headache attacks, although difficult, could support or refute these observations. Nonetheless, advising patients to keep the bedroom cool and avoid other factors that raise body heat may help to reduce frequency and severity of attacks during cluster periods.
(1) Headache classification committee of the International Headache Society. Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia 1988; 8 (suppl 7): 35-37.
(2) Saunte C, Russell D, Sjaastad O. Cluster headache: on the mechanism behind attack-related sweating. Cephalalgia 1993; 3: 175-85.
(3) Sjaastad O. Cluster headache syndome. Philadelphia: Saunders, 1992: 206-16.
(4) May A, Bahra A, Buchel C, Frackowiack RSJ, Goadsby P. Hypothalamic activation in cluster headache attacks. Lancet 1998; 352: 275-78.
(5) Hardebo JE. How cluster headache is explained as an intra-cavernous inflammatory process lesioning sympathetic fibers. Headache 1994; 34: 125-31.
City of London Migraine Clinic, 22 Charterhouse Square, London EC1M 6DX, UK
(J N Blau FRCP, H O Engel FFOM)
Correspondence to: Dr J N Blau
Number of patients
Alcohol 118
Environmental heat 52
Exertion (three by sexual intercourse) 23
No known precipitant 51
82 had one precipitant, 54 had two, and 13 all three precipitants.
Attack precipitants in 200 patients
COPYRIGHT 1999 The Lancet Ltd.
COPYRIGHT 2000 Gale Group