Spinal neuroplasticity in chronic pain

Abstract

Neuroplastic changes play an important role in the generation and maintenance of chronic pain syndromes. Such changes occur at all levels of the neuraxis, from the peripheral terminals of primary sensory neurons to the cerebral cortex. Changes observed in the spinal dorsal horn in particular provide a mechanistic basis for many of the characteristics of chronic pain syndromes. While facilitated synaptic transmission between nociceptive fibers and spinal projection neurons contributes to enhanced perception of noxious stim­uli (hyperalgesia), diminished function of GA­BA-ergic and glycinergic interneurons not only induces hyperalgesia, but also triggers no­ciceptive reactions on exposure to innocuous stimuli and spontaneous pain behavior in the absence of any sensory stimulation. Spinal disinhibition thus recapitulates typical symptoms of chronic pathological pain syndromes. Studies performed by various groups over the last 10 years demonstrate that such spinal disinhibition occurs naturally in response to peripheral inflammation and nerve dam­age. The present article summarizes current status of this research.