Neuroplasticity and chronic pain

Abstract

In the seventies and eighties spinal mechanisms inhibiting pain processing were discovered in animal studies leading to new therapeutic regimens such the use of spinal opioids. During the last decade additional studies revealed an increased sensibility of the spinal cord upon severe, long lasting pain perception, a mechanism called wind-up. Hyperalgesia is accompanied by persisting genetic changes of spinal cord cells, which may contribute to the chronification of pain. The severity and duration of acute pain apparently contributes to the possibility of chronic pain development. Although not all the consequences of these findings are clear, they may influence our way of performing anaesthesia and treating postoperative or acute pain situations, e.g. pain during herpes zoster or pain after trauma and amputation. In general, analgetic measures should be potent enough to prevent spinal sensiblisation, which can be best achieved with spinal blockade by local anesthetics. Another way of counteracting pain-induced spinal plasticity is by blocking or antagonizing its pathways with specific transmitters or their equivalents. All these spinally mediated regimens should be performed prior to later predominating mechanisms of supraspinal plasticity involving psychic changes due to persisting pain, which seem to evolve with delay to spinal processes.