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