Pathophysiology of Pain
To treat pain effectively, it is important to understand the pathophysiology of pain. The International Association for the Study of Pain (IASP) defines pain as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage."
Damaging stimuli are detected by peripheral nociceptors (A-delta and C-fibers) located in skin, muscle, joint, and visceral tissues. The noxious stimuli that activates these fibers may be mechanical, thermal, or chemical. The fibers can be sensitized by endogenous chemicals, such as serotonin, substance P, bradykinin, prostaglandin, and histamine. These sensory receptors send afferent signals through the dorsal horn of the spinal cord, ascending neural pathways, thalamus, limbic areas, and postcentral gyrus, among other cortical areas of the brain, for neural processing.
If you would like to review the neuroanatomical pathway by which pain signals extend into the brain, this is a fun and interactive way to do so from the University of Utah Spencer S. Eccles Health Sciences Library: Anterolateral System Review.
There are three major classes of opioid receptors—mu, kappa, and delta—located in the dorsal horn of the spinal cord and other areas within the peripheral and central nervous system. Opioids bind to these receptors and modulate pain by inhibiting calcium channels and preventing or inducing the release of neurotransmitters that influence the balance of antinociceptive and nociceptive neurotransmitters (e.g., substance P). The mu receptor is likely the most important for analgesia.
Remember, pain is often a combination of sensory, emotional, and cognitive processes, and physical pathology in the form of ongoing tissue-damaging processes need not be present for a patient to experience pain.