J Korean Soc Spine Surg.  2015 Mar;22(1):13-19. 10.4184/jkss.2015.22.1.13.

Neurophysiologic Mechanism of Pain

• Ra IH
• Min WK

• KMID: 1800389
• DOI: http://doi.org/10.4184/jkss.2015.22.1.13

Abstract

STUDY DESIGN: A review of the literature regarding neurophysiologic mechanism of pain.
OBJECTIVES
To review and discuss neurophysiologic mechanism of pain, including neuropathic pain. SUMMARY OF LITERATURE REVIEW: The neurophysiology of pain has been established at the cellular and molecular biology level through many studies. Also, multiple modalities to manage pain have been developed.
MATERIALS AND METHODS
A literature review.
RESULTS
Pain develops by actions of multiple receptors, ion channels and neurotransmitters along the pain pathway. Pathologic states, such as persistent pain, allodynia, and hyperalgesia, arise from alteration of the pain pathway. Especially, neuropathic pain results from nerve injury and its pathology is rather different from the neuroplasty of normal individuals.
CONCLUSION
Multiple modalities, including individualized pain treatment based on pain phenotype, are introduced. However, optimal treatment is uncertain, therefore, further studies are needed.

Keyword

Pathways of pain; Neuroplasticity; Neuropathic pain

MeSH Terms

Hyperalgesia
Ion Channels
Molecular Biology
Neuralgia
Neuronal Plasticity
Neurophysiology
Neurotransmitter Agents
Pathology
Phenotype
Ion Channels
Neurotransmitter Agents

Figure

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  Fig. 1. Physiologic pathways involved in pain sense are composed of transduction, conduction, transmission, modulation, projection, perception.

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  Fig. 2. Large myelinated low-threshold Aβ afferents terminate in laminae III and IV, lightly myelinated high-threshold Aδ fibers synapse at laminae I and V, and non-myelinated high-threshold C fibers terminate in lamina II but also terminate with some fibers in laminae I and V.

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  Fig. 3. Within the DRG, signal transduction cascades are activated, which control the transcription factors that modulate gene expression, leading to changes in the levels of receptors, ion channels, and other structural proteins.

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  Fig. 4. Changes due to the nerve injury increase synaptic input from nociceptor and contribute to an amplification of pain, with a reduction in its threshold and a change in its temporal characteristics. A stimulus from C-fiber of nociceptor increases expression of neuropeptides in Aβ and leads to central sprouting of Aβ. Also, receptors for input from Aβ fiber increase in C-fiber. These phenotypic, structural changes cause central sensitization.

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  Fig. 5. Primary and secondary nociceptive neurons are sensitized by peripheral injury-induced T-cell infiltration and microglia activation in spinal cord. And they raise neuropathic pain.

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