Der Schmerz
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If migraine attacks occur more frequently than 2 times a month, treatment of the acute attack with analgesics and ergotamine becomes problematic. An acute relief of migraine symptoms will be achieved only at the risk of developing a drug-induced chronic headache. Therefore, if migraine attacks occur frequently prophylactic treatment should be considered. ⋯ There is, however, convincing evidence that neither clonidine, nor anti-histamines, nor barbiturates, nor antiepileptic drugs, nor anxiolytics are effective in the prophylactic treatment of migraine. Successful prophylactic treatment cannot be achieved by drug therapy alone. Any form of drug treatment should be complemented by providing the patient with detailed information about the nature of the disease and the properties of the prescribed drugs, as well as careful investigation of the patient's situation and habits and a careful search for precipitants, combined with an attempt to change the patient's habits and to avoid factors that trigger the attacks.
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Sixty-five patients (51 women, 14 men), who were 41.9 years on average, suffered from combination headache (migraine and tension headache) and were under therapy with propranolol and amitriptyline-N-oxide. The following predictive factors were tested with regard to the success of therapy: age, sex, duration of the migraine and tension headache illness, and frequency of use of analgesic and ergotamine preparations. ⋯ Both the migraine treatment and the tension headache were standardized and headache records were kept. The statistical procedure used permitted clear differentiation between responders and non-responders, but these predictive factors did not make it possible to distinguish a subgroup of potential responders.
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Since the beginning of the history of man migraine has been described in all civilizations. It would therefore seem helpful if migraine were to be classified, for diagnostic reasons and in order to study the scientific hypotheses, according to the manifold clinical symptoms, as well as the lack of typical pathophysiological, morphological and biochemical findings. ⋯ On the basis of this classification, the individual forms of migraine are described from the viewpoint of the clinical symptoms. The classification of the International Headache Society represents a good basis for reclassifying headaches, which is still under discussion.
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Migraine is more than the pain involved in the "migraine attack." Before the onset of pain many clinical symptoms can be observed. These symptoms may be classified as vegetative, affective, and vascular. Brain perfusion is altered during migraine attacks as well as during the intervals between attacks. ⋯ It may be assumed that platelet serotonin is a potent vasoregulating substance that may interact in the brain vessels with the neurotransmission controlled perfusion. The hypothesis of an (inborn) instability of the interaction of cerebral neurotransmission systems in patients suffering from migraine is in accordance with the vegetative and affective symptoms in migraine, the observed imbalance of neurotransmission mediated cerebrovascular autoregulation and the irritation of platelets in migraine attacks, as well as in the interval between attacks. The "modern" treatments of migraine with acetylsalicylic acid, ergotamin and/or beta blockers are discussed in relation to this proposed hypothesis of a migraine pathophysiology.
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Pathophysiological models of migraine describe stress as a potential activator of migraine. Clinical observations have shown that stress over prolonged periods leads to migraine, particularly in the relaxation period (e.g. sleep) that follows the stress situations. However, psychophysiological investigations have not been able to prove a direct correlation between stress and the reaction of peripheral and central vascular mechanisms. ⋯ The peripheral resistance was measured by Doppler ultrasonography. The results showed a significant response specificity in migraine patients with respect to peripheral resistance. The results are discussed using a diathesis-stress model of migraine.