Spinal mechanisms contributing to joint pain

Abstract

Nociceptive input from the joint is processed in different types of spinal cord neurons. A proportion of these neurons are only activated by mechanical stimulation of the joint and other deep tissue, e.g. adjacent muscles. Other neurons are activated by mechanical stimulation of joint, muscles and skin. The majority of the neurons are wide dynamic-range neurons (small responses to innocuous pressure to deep tissue and stronger and graded responses to noxious mechanical stimulation). Importantly, neurons with joint input show pronounced hyperexcitability during development of joint inflammation (enhanced responses to mechanical stimulation of the inflamed joint as well as to healthy adjacent deep structures, reduction of mechanical threshold in high threshold neurons and expansion of the receptive field). Thus inflammation induces neuroplastic changes in the spinal cord which alter nociceptive processing. This state of hyperexcitability is maintained during persistent inflammation. The neurons are under strong control of descending inhibition which increases at least during the acute phase of inflammation. Several transmitters and mediators contribute to the generation and maintenance of inflammation-induced spinal hyperexcitability including glutamate, substance P, neurokinin A, CGRP, prostaglandins and probably others. The latter compounds show enhanced release and an altered release pattern during inflammation in the joint.