Cephalalgia : an international journal of headache
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Randomized Controlled Trial Clinical Trial
Responders and non-responders to metoprolol, propranolol and nifedipine treatment in migraine prophylaxis: a dose-range study based on time-series analysis.
The aim of the present study was to ascertain, on the basis of single case statistics and time-series analysis, responder and non-responder rates for metoprolol, propranolol and nifedipine in migraine prophylaxis. In addition, an attempt was made to identify the dose relationship for the various drugs on headache parameters. In a double-blind dose-finding study, 58 patients were treated in five consecutive dosage steps each lasting 1-3 months. ⋯ Higher doses of propranolol and metoprolol were more effective. Multiple regression analysis explained a considerable part of variance for propranolol (but not for metoprolol) as a result of reduced intake of ergotamine preparations and analgesics. It can therefore be concluded that part of the prophylactic effect of propranolol is attributable to a reduction in the use of migraine medication.
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To define the term "menstrual" migraine and to determine the prevalence of "menstrual" migraine in women attending the City of London Migraine Clinic. ⋯ A small percentage of women have attacks only occurring at the time of menstruation, which can be defined as true "menstrual" migraine. This group is most likely to respond to hormonal treatment. The group of 34.5% who have an increased number of attacks at the time of menstruation in addition to attacks at other times of the month could be defined as having "menstrually related" migraine and might well respond to hormonal therapy. The 32.7% who have attacks throughout the menstrual cycle without an increase at menstruation are unlikely to respond to hormonal therapy. The 25.5% who do not have attacks related to menstruation almost certainly will not respond to hormonal therapy.
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The term "cluster vertigo" was originally used by Gilbert to describe episodes of vertigo in patients with Ménière's syndrome. Since these patients also had co-existing cluster headache, he suggested that both disorders could have had a common pathophysiology. There is no evidence in the literature for an increased incidence of Ménière's syndrome in cluster headache patients, so the argument that cluster headache and Ménière's syndrome may have a common pathogenesis cannot be supported. ⋯ This was not the intention of the original author. The terminology is misleading and should not be used to describe a sub-type of cluster headache. A case of cluster headache with accompanying vertigo is described as a contrast to the patients described by Gilbert in whom headache and episodes of vertigo occurred independently.
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Substance P, calcitonin gene-related peptide and vasoactive intestinal polypeptide-like immunoreactivities have been evaluated in the saliva of 15 subjects suffering from migraine without aura and 16 control subjects. All three peptides were also measured in the symptomatic/non-symptomatic side saliva sampled from 10 cluster headache sufferers during the cluster period, 5 cluster headache sufferers out of the cluster period, as well as in the right and left side saliva of 18 control subjects. The most interesting result gives a clear difference in common migraine and cluster headache salivary vasoactive intestinal polypeptide-like immunoreactivity contents. ⋯ Finally, during cluster headache attacks the enhancement of substance P-like immunoreactivity and vasoactive intestinal polypeptide-like immunoreactivity salivary contents interest the non-symptomatic side, whereas the symptomatic side salivary substance P-like immunoreactivity and vasoactive intestinal polypeptide-like immunoreactivity contents remain unchanged. These findings do not allow any final conclusion. However, this biochemical evaluation indicates relevant changes of the salivary neuropeptides in diseases, such as migraine and cluster headache, in which pain transmission is surely involved.
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The purpose of this investigation was to evaluate whether the pain of cervicogenic headache could be due to referred symptoms from myofascial trigger points. The presence or absence of cervical spine dysfunction was also of interest. Eleven patients with cervicogenic headaches were systematically examined for myofascial trigger points and cervical spine dysfunction. ⋯ It is concluded that myofascial trigger points may be an important pain producing mechanism in cervicogenic headache and that segmental cervical dysfunction is a common feature in such patients. Conservative, non-surgical treatment appears to be effective in reducing the frequency and intensity of cervicogenic headache. These data suggest that surgical approaches should be reserved only for those patients who fail conservative therapy.