Der Schmerz
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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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In the present article aspects of reflex sympathetic dystrophy (RSD) and sympathetically maintained pain (SMP) are discussed from the point of view of a basic scientist. The main focus is on the sympathetic nervous system. ⋯ Finally, clinical observations are discussed that seem to bear little or no relation to the models that are available. The general synopsis puts the problem into a wider context.
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The gate-control theory of pain, as originally proposed by Melzack and Wall [8], is nothing but a hypothesis concerning the spinal processing of non-noxious and noxious afferent information. Its basic tenant is that the P cells (projecting neurons) convey noxious information to supraspinal pain systems only after a critical threshold of excitation has been passed, and that access to the P cells is controlled by the SG cells (cells of the substantia gelatinosa Rolandi) or, in other words, the SG cells act as the gate. Since the primary afferent fibres have monosynaptic connections with the P cells the gate can only operate-and this is the critical point of the whole hypothesis-via presynaptic inhibition exerted by axoaxonic contacts on these afferents (Fig. 1). ⋯ As a consequence, Melzack and Wall [9] have now modified their hypothesis considerably. Its present formulation is not much more than a very general statement to the effect that all kinds of afferent input, including noxious input, is under the modulating influence of various mechanisms operating both at the spinal level and from supraspinal (descending) structures. No implications for therapy can be derived directly from such an undefined, in many ways trivial, assumption.