• Adeline Fong and Stephan A Schug.
• Perth, Australia From the Department of Pain Management, Sir Charles Gairdner Hospital; and Pharmacology, Pharmacy and Anaesthesiology Unit, School of Medicine and Pharmacology, The University of Western Australia.
• Plast. Reconstr. Surg. 2014 Oct 1; 134 (4 Suppl 2): 8S-14S.

SummaryThe experience of pain is a subjective one and more than a simple sensation. Pain is commonly defined as an unpleasant sensory and emotional experience due to actual or potential tissue damage or described in such terms. Pain may be broadly classified into physiological and pathological pain. Nociceptive and inflammatory pains are physiological pain states, as they are protective and adaptive, whereas pathological pain is nonprotective and maladaptive. Nociception is the result of suprathreshold stimulation of peripheral nociceptors. Inflammatory pain follows release of various chemical mediators after tissue injury including surgery leading to peripheral sensitization. Nociceptive input is then transmitted to the spinal cord via primary afferents. Modulation of the nociceptive input occurs in the dorsal horn of the spinal cord, influenced by descending inhibitory systems. Central sensitization is a neuromodulatory change that results in the development of secondary hyperalgesia. The modulated nociceptive input then travels up the ascending tracts, mainly via the spinothalamic tract to the thalamus and subsequently to the higher centers of the brain. Pathological pain such as neuropathic pain and central nervous system dysfunctional pain are the result of neuroplasticity of the peripheral and central nervous system. Abnormal ectopic firing of neurons in the absence of a stimulus, increased neuronal hypersensitivity, changes within ion channels, and even alteration in gene expression and changes in the cortical representation are involved in the pathogenesis of these pain states. The development of persistent postsurgical pain is an example for this complex process.

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