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Peripheral Autonomic Neuropathies
Published in David Robertson, Italo Biaggioni, Disorders of the Autonomic Nervous System, 2019
Numerous pain mechanisms associated with the sympathetic nervous system have been recognized. It is clear that under normal physiological conditions the efferent sympathetic nervous system is not involved in pain perception. Nevertheless, the sympathetic nervous system is involved in response to threatening, damaging signals from the periphery or viscera. These reactions have biological significance. After injury, particularly that involving limbs with or without direct lesions to nerves, additional reactions to injury which involve a number of mechanisms bring the efferent sympathetic nervous system into play as a causative or permissive component in pain generation and its associated processes. Evidence that postganglionic noradrenergic fibres influence nociceptors that supply the extremities has emerged. This mechanism depends on several different conditions in the periphery that may operate singly or together. Chemical coupling is thought to be a well-established pathophysiological mechanism for some form of neuropathic pain. Ephaptic coupling between postganglionic and somatic afferent axons is still only hypothetical, but indirect coupling through alterations in the microenvironment of nociceptors, for example, causing a sensitization, is thought to be a likely mechanism by which the sympathetic nervous system acts as a promoter of afferent pain. Components that together change the neurovascular transmission are thought to be important in this mechanism (Janig, 1989).
Reorganization of synaptic inputs to spinal dorsal horn neurons in neuropathic pain
Published in International Journal of Neuroscience, 2022
Development of neuropathic pain is typically a result of various structural and functional changes in damaged peripheral nerve fibers, the spinal dorsal horn, and pain-associated brain regions. Injured nerves become abnormally excitable and produce an ectopic discharge by axonal disruption in the neuroma and ephaptic coupling between injured primary neurons [3, 4]. These changes may promote the release of neurotransmitters or other substances, such as ATP, tissue necrosis factor-α (TNF-α), and fractalkine, from the central terminal sites of primary afferents in the spinal dorsal horn [5–9]. As a result, a variety of functional and morphological changes occur in the spinal dorsal horn as well as in the injured nerves, contributing to the development and pathogenesis of neuropathic pain. Below, we briefly review changes in the spinal dorsal horn related to reorganization of the synaptic network after peripheral nerve injury. Dysfunction of inhibitory interneurons, activation of glial cells, changes in neuronal excitability, and convergent nociceptive inputs to secondary neurons in the spinal dorsal horn are discussed.