Yeungnam Univ J Med.  2000 Jun;17(1):12-20. 10.12701/yujm.2000.17.1.12.

Memory of Pain and Preemptive Analgesia

Affiliations
  • 1Department of Anesthesia and Pain Medicine College of Medicine, Yeungnam University, Taegu, Korea.

Abstract

The memory of pain can be more damaging than its initial experience. Several factors are related the directions of pain memory; current pain intensity, emotion, expectation of pain, and peak intensity of previous pain. The possible mechanisms of memory of pain are neuroplastic changes of nervous system via peripheral and central sensitization. Peripheral sensitization is induced by neurohumoral alterations at the site of injury and nearby. Biochemicals such as K+, prostaglandins, bradykinin, substance P, histamine and serotonin, increase transduction and produce continuous nociceptive input. Central sensitization takes place within the dorsal horn of spinal cord and amplifies the nociceptive input from the periphery. The mechanisms of central sensitization involve a variety of transmitters and postsynaptic mechanisms resulting from the activations of NMDA receptors by glutamate, and activation of NK-1 tachykinnin receptors by substance-P and neurokinnin. The clinical result of peripheral and central sensitization is hyperalgesia, allodynia, spontaneous pain, referred pain, or sympathetically maintained pain. These persistent sensory responses to noxious stimuli are a form of memory. The hypothesis of preemptive analgesia is that analgesia administered before the painful stimulus will prevent or reduce subsequent pain and analgesic requirements in comparison to the identical analgesic intervention administered after the painful stimulus, by preventing or reducing the memory of pain in the nervous system. Conventionally, pain management was initiated following noxious stimuli such as surgery. More recently, many have endorsed preemptive analgesia initiated before surgery. Treatments to control postsurgical pain are often best started before injury activates peripheral nociceptors and triggers central sensitization. Such preemption is not achieved solely by regional anesthesia and drug therapy but also requires behavioral interventions to decrease anxiety or stress. Although the benefit of preemptive analgesia is not obvious in every circumstance, and in many cases may not sufficient to abolish central sensitization, it is an appropriate and human goal of clinical practice.

Keyword

Central sensitization; Memory of pain; Preemptive analgesia

MeSH Terms

Analgesia*
Anesthesia, Conduction
Animals
Anxiety
Bradykinin
Central Nervous System Sensitization
Drug Therapy
Glutamic Acid
Histamine
Horns
Humans
Hyperalgesia
Memory*
Nervous System
Nociceptors
Pain Management
Pain, Referred
Prostaglandins
Receptors, N-Methyl-D-Aspartate
Serotonin
Spinal Cord
Substance P
Bradykinin
Glutamic Acid
Histamine
Prostaglandins
Receptors, N-Methyl-D-Aspartate
Serotonin
Substance P
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