Pain reception and transmission

The Pathophysiology of Pain

Pain reception and transmission

Nociceptive Reception and Transmission

Nociceptive pain occurs as a result of the activation of the nociceptive system by noxious stimuli, inflammation or disease.1,2

 

The neurophysiologic underpinnings of pain can be divided into four stages: transduction, transmission, pain modulation, and perception.3  At every point in the process, the intensity and propagation of pain signals can be either inhibited or facilitated by neural pathways originating in the brain. This capacity to modulate signaling may account, in part, for wide variations in pain perception between different individuals who sustain the same injury.4

 

Transduction

Transduction occurs when a stimulus, such as pressure, thermal energy, or chemical irritation, is converted into a nerve signal (e.g., an action potential). This occurs at the ends of sensory nerve cells (nociceptors) whose terminals are sensitive to this type of activation.5  These nociceptors are distributed throughout the body.6

 

Transmission

Transmission is the process of transferring pain information from the peripheral to the central nervous system.7 Signals are transmitted along the axons of nociceptors. These small-diameter nerve fibers comprise two main types: unmyelinated C-fibers, which conduct impulses slowly and thinly myelinated A-delta fibers, which carry impulses at a faster rate.8,9 Most primary sensory nerve fibers, including nociceptors, synapse with second-order neurons in the dorsal horn of the spinal cord. From here, projection neurons carry information to the brainstem, thalamus, and hypothalamus, as well as to reflex arcs to mediate an avoidance response.10

 

Modulation 

Pain modulation refers to the transmission of pain signals through the dorsal horn.11  Many of these signals never reach consciousness because they are dampened by intrinsic modulatory activity within the central nervous system.12 The gate control theory, advanced by Melzack and Wall in 1962, focused on descending pathways from the brain to the spinal cord that inhibited pain signaling.13 The current view is that signals originating in the brain can both inhibit and facilitate pain signal transmission.14   Neurotransmitters involved in these pathways include endogenous opiates (enkephalins, dynorphins, beta-endorphins),15 serotonin, and norepinephrine.

 

Perception

Perception of pain is the awareness—typically an uncomfortable awareness—associated with a specific area of the body. It depends on the transmission of pain signals through the thalamus to the cortex and limbic system.16 At this point in pain processing, perception of the pain experience is influenced by social and environmental cues, as well as by cultural conditioning and past personal experiences.17

 

Some Etiologies of Nociceptive Pain

  • Musculoskeletal Injuries
  • Tissue Damage
  • Post-surgical Nociceptive Pain
  • Cancer-related Nociceptive Pain
  • Myofascial Pain Syndrome

1Woolf CJ. Pain: moving from symptom control toward mechanism-specific pharmacologic management. Ann Intern Med. 2004;140:441-451.
2Woolf CJ, Salter MW. Neuronal plasticity: increasing the gain in pain. Science. 2000;288:1765-1768.
3National Pharmaceutical Council and Joint Commission on Accreditation of Healthcare Organizations. Pain: Current Understanding of Assessment, Management, and Treatments. Reston, VA: National Pharmaceutical Council; 2001.
4National Pharmaceutical Council and Joint Commission on Accreditation of Healthcare Organizations. Pain: Current Understanding of Assessment, Management, and Treatments. Reston, VA: National Pharmaceutical Council; 2001.
5National Pharmaceutical Council and Joint Commission on Accreditation of Healthcare Organizations. Pain: Current Understanding of Assessment, Management, and Treatments. Reston, VA: National Pharmaceutical Council; 2001.
6Hudspith MJ, Siddall PJ, Munglani R. Physiology of pain. In: Hemming HC, Hopkins PM, eds. Foundations of Anesthesia. 2nd ed. London, UK: Mosby; 2006:267-285.
7Hudspith MJ, Siddall PJ, Munglani R. Physiology of pain. In: Hemming HC, Hopkins PM, eds. Foundations of Anesthesia. 2nd ed. London, UK: Mosby; 2006:267-285.
8Hudspith MJ, Siddall PJ, Munglani R. Physiology of pain. In: Hemming HC, Hopkins PM, eds. Foundations of Anesthesia. 2nd ed. London, UK: Mosby; 2006:267-285.
9Carver A. Pain. In: Dale DC, Federman DD, eds. ACP Medicine. New York, NY: WebMD; 2005:1-18.
10Carver A. Pain. In: Dale DC, Federman DD, eds. ACP Medicine. New York, NY: WebMD; 2005:1-18.
11Hudspith MJ, Siddall PJ, Munglani R. Physiology of pain. In: Hemming HC, Hopkins PM, eds. Foundations of Anesthesia. 2nd ed. London, UK: Mosby; 2006:267-285.
12Carver A. Pain. In: Dale DC, Federman DD, eds. ACP Medicine. New York, NY: WebMD; 2005:1-18.
13Melzack R, Wall PD. Pain mechanisms: a new theory. Science. 1965;150(3699):971-979.
14Hudspith MJ, Siddall PJ, Munglani R. Physiology of pain. In: Hemming HC, Hopkins PM, eds. Foundations of Anesthesia. 2nd ed. London, UK: Mosby; 2006:267-285.
15Carver A. Pain. In: Dale DC, Federman DD, eds. ACP Medicine. New York, NY: WebMD; 2005:1-18.
16Hudspith MJ, Siddall PJ, Munglani R. Physiology of pain. In: Hemming HC, Hopkins PM, eds. Foundations of Anesthesia. 2nd ed. London, UK: Mosby; 2006:267-285.
17Hudspith MJ, Siddall PJ, Munglani R. Physiology of pain. In: Hemming HC, Hopkins PM, eds. Foundations of Anesthesia. 2nd ed. London, UK: Mosby; 2006:267-285.