A brief comparison of the pathophysiology of inflammatory versus neuropathic pain

Abstract

Purpose of review: The causes of inflammatory pain and neuropathic pain are fundamentally different. There are, however, common mechanisms underlying the generation of each pain state. We will discuss some specific elements observed in both tissue and nerve injury pain states and consider the hypothesis that these two states actually demonstrate a convergence over time.

Recent findings: The increased pain sensation following tissue and nerve injury results from several mechanisms, including altered ion channel expression in dorsal root ganglion neurons, enhanced dorsal horn glutamate release from primary afferents, enhanced glutamate receptor function in second-order neurons, disinhibition in the dorsal horn and glia cell activation. The role of specific subtypes of receptors, ion channels and glutamate transporters is revealed at peripheral and central sites. Importantly over time, a number of changes, in the dorsal root ganglion and in dorsal horn observed after tissue injury resemble changes observed after nerve injury.

Summary: Recognition of mechanisms common to both inflammatory pain and neuropathic pain might shed light on the understanding of the transition from acute pain to persistent pain.

Fig 1. Mechanims mediating persistent pain following tissue injury or nerve injury

Following tissue injury or nerve injury, pathological changes that might lead to persistent pain in the DRG (1) and the spinal cord dorsal horn (2). Common mechanisms are listed in the gray boxes. See text for details. ATF3, cyclic AMP-dependent transcription factor; TNF, tumor necrosis factor; TNFr, tumor necrosis factor receptor.