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WIREs Cogn Sci
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Abstract Pain has many valuable functions. It often signals injury or disease, generates a wide range of adaptive behaviors, and promotes healing through rest. Despite these beneficial aspects of pain, there are negative features that challenge our understanding of the puzzle of pain, including persistent phantom limb pain after amputation or total spinal cord transection. Pain is a personal, subjective experience influenced by cultural learning, the meaning of the situation, attention, and other psychological variables. Pain processes do not begin with the stimulation of receptors. Rather, injury or disease produces neural signals that enter an active nervous system that (in the adult organism) is the substrate of past experience, culture, and a host of other environmental and personal factors. These brain processes actively participate in the selection, abstraction, and synthesis of information from the total sensory input. Pain is not simply the end product of a linear sensory transmission system; it is a dynamic process that involves continuous interactions among complex ascending and descending systems. The neuromatrix theory guides us away from the Cartesian concept of pain as a sensation produced by injury, inflammation, or other tissue pathology and toward the concept of pain as a multidimensional experience produced by multiple influences. These influences range from the existing synaptic architecture of the neuromatrix—which is determined by genetic and sensory factors—to influences from within the body and from other areas in the brain. Genetic influences on synaptic architecture may determine—or predispose toward—the development of chronic pain syndromes. WIREs Cogn Sci 2013, 4:1–15. doi: 10.1002/wcs.1201 This article is categorized under: Psychology > Brain Function and Dysfunction

Schematic representation of conceptual models of pain mechanisms. (a) Specificity theory. Large (L) and small (S) fibers are assumed to transmit touch and pain impulses, respectively, in separate, specific, straight‐through pathways to touch and pain centers in the brain. (b) Goldscheider's7 summation theory, showing convergence of small fibers onto a dorsal horn cell. The central network projecting to the central cell represents Livingston's5 conceptual model of reverberatory circuits underlying pathological pain states. Touch is assumed to be carried by large fibers. (c) Sensory interaction theory, in which large (L) fibers inhibit (−) and small (S) fibers excite (+) central transmission neurons. The output projects to spinal cord neurons, which are conceived by Noordenbos8 to comprise a multisynaptic afferent system. (D) Gate control theory. The large (L) and small (S) fibers project to the substantia gelatinosa (SG) and first central transmission (T) cells. The central control trigger is represented by a line running from the large fiber system to central control mechanisms, which in turn project back to the gate control system. The T cells project to the entry cells of the action system. +, excitation; −, inhibition. (Reprinted with permission from Ref 9. Copyright 1991 Elsevier Ltd)

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Factors that contribute to the patterns of activity generated by the body‐self neuromatrix, which is comprised of sensory, affective, and cognitive neuromodules. The output patterns from the neuromatrix produce the multiple dimensions of pain experience, as well as concurrent homeostatic and behavioral responses. (Reprinted with permission from Ref 21. Copyright 2001 Sage Publications)

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Conceptual model of the sensory, motivational, and central control determinants of pain. The output of the T (transmission) cells of the gate control system projects to the sensory‐discriminative system and the motivational‐affective system. The central control trigger is represented by a line running from the large fiber system to central control processes; these, in turn, project back to the gate control system, and to the sensory‐discriminative and motivational‐affective systems. All three systems interact with one another, and project to the motor system. (Reprinted with permission from Ref 13. Copyright 1968 Charles C Thomas Publisher Ltd)

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