Abstract

Pain has been considered as a concept of sensation that we feel as a reaction to the stimulus of our surrounding, putting us in harm’s way and acting as a form of defense mechanism that our body has permanently installed into its system. However, pain leads to a huge chunk of finances within the healthcare system with continuous rehabilitation of patients with adverse pain sensations, which might reduce not only their quality of life but also their productivity at work setting back the pace of our economy. It may not look like a huge deal but factor in pain as an issue for majority of us, it becomes an economical burden. Although pain has been researched into and understood by numerous researches, from its definition, mechanism of action to its inhibition in hopes of finding an absolute solution for victims of pain, the pathways of pain sensation, neurotransmitters involved in producing such a sensation are not comprehensively reviewed. Therefore, this review article aims to put in place a thorough understanding of major pain conditions that we experience—nociceptive, inflammatory and physiologically dysfunction, such as neuropathic pain and its modulation and feedback systems. Moreover, the complete mechanism of conduction is compiled within this article, elucidating understandings from various researches and breakthroughs.

Highlights

  • Pain is considered to be a human primate instinct and can be defined as a distressing sensation, as well as an emotional experience that is linked to actual or potential tissue damage, with the sole purpose of notifying the body’s defence mechanism to react towards a stimulus in order to avoid further tissue damages

  • This leads to brief pulses generated within the neuron, known as an action potential, which propagate from the soma, travel along the axons to activate the synapses, and are sent to other neurons, acting as a pathway to carry the signals from its source to either the spinal cord or the brain, where a response is interpreted to be executed

  • Due to pain messengers attaching to receptors around the injury site, it causes the sensitization of the adjacent uninjured tissue to the mechanical stimuli, which is commonly known as secondary hyperalgesia or allodynia

Read more

Summary

Introduction

Pain is considered to be a human primate instinct and can be defined as a distressing sensation, as well as an emotional experience that is linked to actual or potential tissue damage, with the sole purpose of notifying the body’s defence mechanism to react towards a stimulus in order to avoid further tissue damages. The sensation of pain is associated with the activation of the receptors in the primary afferent fibers, which is inclusive of the unmyelinated C-fiber and myelinated Aσ-fiber. Internationally pain has been classified into three major classes—nociceptive pain, neuropathic pain and inflammatory pain [1] Both the CNS and PNS are involved in the mechanism and pathways of all variations of pain perception. The PNS comprises nerves and ganglia that are located outside the brain and spinal cord, mainly functioning to connect the CNS to organs and limbs in our body. The CNS is composed of the spinal cord and the brain, which is mainly responsible for integrating and intepreting the information sent from the PNS, and subsequently coordinating all the activities in our bodies, before sending response towards the effector organs

Basic Mechanisms of Pain
Neurons
Group A
Group C
Action Potential
Synaptic Transmission
Route of Pain Transmission
Nociceptive Pain
Neuropathic Pain
Inflammatory Pain
Arthritis
Hyperalgesia
Allodynia
Peripheral Sensitization
Central Sensitization
Neurogenic-Induced Inflammation
Major Types of Pain-Mediated Neurotransmitters
Exert synergistic interaction with NGF and PG
Exert synergistic interaction with NGF
Tachykinins
Calcitonin Gene-Related Peptide
Bradykinin
Cytokines
Prostaglandins
Leukotriene B4
Proton
Adenosine Triphosphate
Nerve Growth Factor
9.10. Glutamate
9.12. Opioid Peptides
9.13. Cannabinoids
9.14. Norepinephrine
Findings
10. Conclusions
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call