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Causalgia, Pathological Pain, and Adrenergic Receptors
Pages 7664-7667

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From page 7664...
... Similar partial denervations also produce a substantial increase in the number of dorsal root ganglion neurons evidencing the presence of a-adrenergic receptors. The hypothesis proposes the increased presence of c'-adrenergic receptors in primary afferent neurons to result from an altered gene expression triggered by cytokines/growth factors produced by disconnection of peripheral nerve fibers from their cell bodies.
From page 7665...
... Adrenergic Receptors and Primary Afferent Neurons. Thus, the events unleashed by a partial denervation, consisting of interruption of some peripheral sensory fibers and/or postganglionic sympathetic fibers, alter the phenotype of nociceptors that otherwise remain functionally intact in the injured or another nerve supplying the region.
From page 7666...
... These human data suggest that a process akin to denervation supersensitivity may operate in classical causalgia and possibly other varieties of sympathetically related pain disorders. To repeat, my suggestion here is that primary afferent neuron excitation by adrenergic agents in classical causalgia results from novel or-adrenergic receptor production in dorsal root ganglia neurons evoked by direct and indirect effects of injury to peripheral innervation.
From page 7667...
... A similar process could operate in other versions of sympathetically related pain. It could also relate to Raynaud's disease, another pathological process which, in part, appears to represent overreaction to sympathetic mediators and could possibly result from an increased expression of adrenergic receptors (37~.


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