Clinically relevant pain states are usually characterized as either inflammatory or neuropathic. While inflammatory pain results from tissue injury or damage, neuropathic pain results from damage or disease of nerve fibers. In either pain state, both the peripheral and the central nociceptive system contribute significantly to the generation of pain. ⋯ Central sensitization is a neuronal process that amplifies the activity from the periphery. Numerous molecular mechanisms are involved in peripheral and central nociceptive processes including rapid functional changes of signaling (increase of excitability) and long-term regulatory changes such as upregulation of mediator/receptor systems. The conscious pain is generated by thalamocortical networks that produce both sensory discriminative and affective components of the pain response.
Abteilung Neurophysiologie, Institut für Physiologie, Klinikum der FSU Jena, Teichgraben 8, 07740, Jena. Hans-Georg.Schaible@mti.uni-jena.de
Orthopade. 2007 Jan 1;36(1):8, 10-2, 14-6.
AbstractClinically relevant pain states are usually characterized as either inflammatory or neuropathic. While inflammatory pain results from tissue injury or damage, neuropathic pain results from damage or disease of nerve fibers. In either pain state, both the peripheral and the central nociceptive system contribute significantly to the generation of pain. During inflammation peripheral nociceptors ("pain fibers") are sensitized (peripheral sensitization), and upon nerve injury or nerve disease peripheral nerve fibers develop ectopic discharges originating from the site of the nerve lesion or the cell body of damaged fibers. As a consequence a complex neuronal response is evoked in the spinal cord where neurons become hyperexcitable (central sensitization).Central sensitization is a neuronal process that amplifies the activity from the periphery. Numerous molecular mechanisms are involved in peripheral and central nociceptive processes including rapid functional changes of signaling (increase of excitability) and long-term regulatory changes such as upregulation of mediator/receptor systems. The conscious pain is generated by thalamocortical networks that produce both sensory discriminative and affective components of the pain response.