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In recent years, the most important contribution to our understanding of pain has been the discovery of a neuronal analgesia system which can be activated by the administration of opiates or by naturally occurring brain substances that share the properties of opiates. This endogenous system was rst demonstrated by Reynolds, who found that stimulation of the ventrolateral periaqueductal gray matter in the rat produced a profound analgesia without altering behavior or motor activity. Subsequently, stimulation of other discrete sites in the medial and caudal regions of the diencephalon and rostral bulbar nuclei (notably raphe magnus and paragigantocellularis) were shown to have the same effect. Under the in uence of such electrical stimulation, the animal could be operated upon without anesthesia and move around in an undisturbed manner despite the administration of noxious stimuli. Investigation disclosed that the effect of stimulation-produced analgesia (SPA) is to inhibit the neurons of laminae I, II, and V of the dorsal horn, i.e., the neurons that are activated by noxious stimuli. In human subjects, stimulation of the midbrain periaqueductal gray matter through stereotactically implanted electrodes has also produced a state of analgesia, though not consistently. Other sites in which electrical stimulation is effective in suppressing nociceptive responses are the rostroventral medulla (nucleus raphe magnus and adjacent reticular formation) and the dorsolateral pontine tegmentum. These effects are relayed to the dorsal horn gray matter via a pathway in the dorsolateral funiculus of the spinal cord. Ascending pathways from the dorsal horn, conveying noxious somatic impulses, are also important in activating the modulatory network. As indicated earlier, opiates also act pre- and postsynaptically on the neurons of laminae I and V of the dorsal horn, suppressing afferent pain impulses from both the A- and C bers. Furthermore, these effects can be reversed by the narcotic antagonist naloxone. Interestingly, naloxone can reduce some forms of stimulationproduced analgesia. Levine and colleagues have demonstrated that not only does naloxone enhance clinical pain but it also interferes with the pain relief produced by placebos. These observations suggest that the heretofore mysterious bene cial effects of placebos (and perhaps of acupuncture) may be due to activation of an endogenous system that shuts off pain through the release of painrelieving endogenous opioids, or endorphins (see below). Prolonged pain and fear are the most powerful activators of this endogenous opioid-mediated modulating system. The same system is probably operative under a variety of other stressful conditions; for example, some soldiers, wounded in battle, require little or no analgesic medication ( stress-induced analgesia ). The opiates also act at several loci in the brainstem, at sites corresponding with those producing analgesia when stimulated electrically and generally conforming to areas in which neurons with endorphin receptors are localized.
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We could shrink it by making each division represent, say, 5 units on both axes. But then the solutions wouldn t show up well; they d be too close together. In situations like this, the best approach is to use rectangular coordinates, but not strict Cartesian coordinates. Let s make each increment on the x axis represent 1 unit, and each increment on the y axis represent 5 units. When we make the axis increments different in size, we distort the slopes and contours of the lines and curves, but that s not important here. Our goal is only to get a good fit for the ranges of the values we determined when we created Table 28-1, and a clear picture of how the graphs intersect. To begin, we plot the two solution points.
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In this case, B is a proper subset of A. That s because every element in B is also in A, but there are some elements in A that are not in B. We write this fact as B A.
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