Der Schmerz
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This study presents the first-ever account of the prevalence of headache syndromes in Germany and the frequency with which they occur in a large representative sample according to the International Headache Society criteria, as set out in the German translation approved by the Classification Committee. 5000 persons representative of the total population were selected from a panel of 30000 households and requested to answer a questionnaire about headache occurrence during their life to date (lifetime prevalence). Of the 5000 persons who were sent questionnaires, 81.2% (n=4061) completed and returned them: 71.4% (n=2902) said they suffered from headache at least occasionally. Of the base population (all respondents: 100% orn=4061), 27.5% (n=1116) fulfilled the criteria for the IHS classification ofmigraine, 38.3% (n=1557) displayed the criteria oftension headache and 5.6% (n=229) said they suffered from headaches, but did not fulfil the criteria for either migraine or tension headache and were therefore classified in the category other headache. ⋯ The importance of the neurological disorders migraine and tension headache is currently seriously underestimated. They are one of the major health problems of our time. There is an urgent need for much greater attention to them by the health system.
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Several studies of contingent negative variation (CNV) examined whether this method provides a suitable basis for research on pathogenetic processes in chronic headaches-especially migraine. In the present study, the CNV amplitudes and CNV course of 23 migraine patients were compared with those of 22 healthy subjects. CNV was calculated for (a) "total interval", (b) "early CNV component", and (c) "late CNV component". ⋯ The results allow the assumption that the higher level of CNV amplitude in migraine patients is not only due to higher cortical noradrenergic or serotoninergic activation. This study shows that migraine patients cannot decrease their CNV amplutides. This is probably due to defective processing of sensory imput.
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This paper reviews several recently developed animal models that allow a quantitative assessment of the magnitude of nocifensive behavioral responses across a range of noxious stimulus intensities. Models discussed in detail include: (a) the rodent tail flick reflex, and a modification that allows measurement of tail flick magnitude, (b) rat hindlimb flexion withdrawal reflex elicited by noxious thermal stimulation of the paw, and (c) a learned operant response (nose bar press) evoked by noxious thermal stimulation of the rat's tail. These models are discussed in terms of their advantages over previous methods measuring response threshold, their fulfillment of criteria for ideal pain assessment models, and the neuronal circuitry underlying the behavioral response.
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The quantitative approach to the study of descending inhibition of spinal nociceptive transmission was initiated in Heidelberg through the use of natural, noxious stimulation and examination of the modulation of the encoding properties of spinal dorsal horn neurons. This important approach required control of the noxious stimulus, which had previously been inadequately considered, and the parametric assessment of modulatory influences on the encoding properties of spinal dorsal horn neurons. As a consequence, descending inhibition of spinal nociceptive transmission was found not to be homogeneous throughout the brainstem, but rather to be significantly different from different brainstem nuclei. ⋯ Most recently, the same approach has been profitably applied to studies that have focused onfacilitatory influences descending from many of the same brainstem sites. As a consequence, it has been proposed that there exists an endogenous pain facilitating system analogous to the well-accepted endogenous pain inhibitory system. While the function of the facilitatory system remains unknown, it is proposed that it may be important to long-lasting pain conditions that exist in the absence of pathology.
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Prolonged administration of morphine for the treatment of chronic pain causes constipation requiring the use of laxatives, which may result in electrolyte deficits. Morphine-induced constipation is due to the binding of the drug to opioid receptors in the gastrointestinal tract and the brain, where it mimics the actions of enkephalins. The effect on the gastrointestinal tract seems to be more intense than the central effect. ⋯ Provided that the anatomical organization of the haemorrhoidal veins in the rat is similar to that in man, slow-release naloxone will be carried by the matrix, to which it is absorbed further down in the gastrointestinal tract. It may thus even reach the rectum, from where, after having been absorbed, it bypasses the liver, enters the central nervous system and reduces the antinociceptive effect of morphine. In conclusion, it can be stated that oral administration of naloxone in combination with morphine may help to prevent constipation during the treatment of chronic pain.