SUMMARY The cyclic nature of cluster headache warranted a study of the 24-hour rhythms of serum cortisol and melatonin. They were both altered during cluster periods as compared with periods of remission and healthy controls. The 24-hour mean and maximal cortisol levels were higher and the timing of the cortisol minimum was delayed as compared to the same patients in remission. Although there was no relation between the cortisol and melatonin levels and headaches, the rise of cortisol following many attacks might in part represent an adaptive response to pain. The nocturnal melatonin maximum was lower during cluster periods than in remission. This finding, and the dysautonomic signs during attacks, may reflect a change of the vegetative tone in a hyposympathetic direction.The cyclic nature of cluster headache and dysautonomic signs during attacks may suggest a dysfunction in the central nervous system related to rhythm-regulating centres. Recently, increasing interest has been focused on changes in hormonal biological rhythms in cluster headache patients.'-9 The pineal hormone melatonin is influenced by bright light'0 and is believed to reflect the circadian organisation of biological rhythms in several species including man. " Serum cortisol also exhibits a circadian rhythm. A functional relation between the pineal gland and the hypothalamic-pituitary-adrenal axis has been suggested.'2 13 We recently reported that the nocturnal levels of serum melatonin were lower in cluster headache during the active headache period than during the remission state.7 Decreased nocturnal serum melatonin levels in patients in an active cluster period as compared to normal healthy controls have also been reported.8 In the present paper the 24-hour rhythms of serum cortisol and melatonin were studied in cluster headache patients during active cluster periods and remissions. Furthermore, the nocturnal urinary excretion of melatonin was examined in cluster headache and healthy control subjects. Patients and methodsStudy ofserum cortisol and melatonin Patients Thirty-one cluster headache patients were admitted to the hospital for the study during the years 1981 to 1984. They were diagnosed as suffering from episodic cluster headache (n = 27) according to Ekbom'4 or as chronic cluster headache (n = 4) according to Ekbom and Olivarius."The age distribution and some anamnestic data are summarised in table 1.Serum cortisol was examined in all 31 patients. Eleven males and five females of the episodic cases were examined both during and between periods ofcluster headache. Serum melatonin was studied in 20 episodic and four chronic cluster patients. From nine of the 20 patients with episodic cluster headache data were obtained both during a cluster period and during a remission. Some data from eight out of these nine patients have been reported previously.7When examined during the remission period all patients were free of medication. During the active cluster period prophylactic therapy (methysergide, pizotifen, ergotamine tartrate) was st...
Five hundred and fifty-four patients with episodic cluster headache (ECH) and chronic cluster headache (CCH) were examined between 1963 and 1997. Mean age at onset was significantly higher in women with CCH compared with women with ECH and in men with ECH or CCH. In women with CCH age at onset was evenly distributed from 10 to 69 years, whereas in men with CCH and in both sexes with ECH, there was a peak when they were in their 20s. In women with ECH a second peak of onset occurred in their 50s. Although not statistically significant, primary CCH started later in women (mean 50.8 years) than secondary CCH (mean 35.5 years). There was a significant variation in the male : female ratio with respect to age at onset, being largest between 30 and 49 years of age (ECH 7.2 : 1; CCH 11.0 : 1) and lowest after 50 (ECH 2.3 : 1; CCH 0.6 : 1). During the observation period of more than 30 years there was a trend towards a decreasing male preponderance; the male : female ratio was significantly higher among patients with onset before rather than after 1970. The proportion of episodic vs. chronic CH did not change during the study period. The nature of the sex- and age-related pattern of cluster headache onset remains to be elucidated but mechanisms associated with sex hormone regulation, perhaps of hypothalamic origin, may be involved, as well as environmental factors related to lifestyle.
Background The aim of this study was to investigate clinical features of a cluster headache cohort in Sweden and to construct and test a new scale for grading severity. Methods Subjects were identified by screening medical records for the ICD 10 code G44.0, that is, cluster headache. Five hundred participating research subjects filled in a questionnaire including personal, demographic and medical aspects. We constructed a novel scale for grading cluster headache in this cohort: The Cluster Headache Severity Scale, which included number of attacks per day, attack and period duration. The lowest total score was three and the highest 12, and we used the Cluster Headache Severity Scale to grade subjects suffering from cluster headache. We further implemented the scale by defining a cluster headache maximum severity subgroup with a high Cluster Headache Severity Scale score ≥ 9. Results A majority (66.7%) of the patients reported that attacks appear at certain time intervals. In addition, cluster headache patients who were current tobacco users or had a history of tobacco consumption had a later age of disease onset (31.7 years) compared to non-tobacco users (28.5 years). The Cluster Headache Severity Scale score was higher in the patient group reporting sporadic or no alcohol intake than in the groups reporting an alcohol consumption of three to four standard units per week or more. Maximum severity cluster headache patients were characterised by higher age at disease onset, greater use of prophylactic medication, reduced hours of sleep, and lower alcohol consumption compared to the non-cluster headache maximum severity group. Conclusion There was a wide variation of severity grade among cluster headache patients, with a very marked impact on daily living for the most profoundly affected.
Forty-nine out of 51 consecutive male patients with episodic cluster headache were studied with regard to their smoking and drinking habits in general and in relation to cluster headache periods. Questionnaires were constructed for data regarding tobacco intake. Situation-related smoking behavior was registered according to Frith (1971). Screening for alcohol over-consumption was made using the Malmö modification of the brief Michigan Alcoholism Screening Test (Mm-MAST). Eighty-three percent of the patients used tobacco on a regular basis at the time of the study, with an average consumption of 20 cigarettes per day. Only 3% had never used tobacco regularly. The smoking-related desire to smoke in different situations was consistent with what is found in a general population of smokers. Sixty-seven percent of the patients had scores on the Mm-MAST indicative of alcohol over-consumption (i.e. heavy social drinking or alcoholism). During active headache periods 79% decreased their alcohol intake, whereas no consistent change in tobacco consumption was reported for the group as a whole. These findings were further corroborated by the fact that alcohol, but not tobacco intake, was reported by the majority of patients to elicit headache attacks during periods. Thus, our study showed high alcohol and tobacco consumption to be prominent features in male patients with episodic cluster headache. Since neither alcohol nor tobacco appear to have properties of ameliorating headache periods or attacks, the addictive behavior in our patients more likely reflects certain personality characteristics.
Migraine patients often report intolerance to odours. Migraineurs report odours may trigger attacks, that they experience osmophobia during attacks, and olfactory hypersensitivity between attacks. In this paper we discuss olfactory mechanisms in migraine. We also present data from a pilot questionnaire study in a group of young women diagnosed with migraine. The study results confirm that hypersensitivity to odour is a common feature in women with migraine. Migraine pathophysiology likely explains this particular vulnerability. We discuss these pathophysiologic mechanisms and hypotheses relating odour intolerances and migraine.
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