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Pain, Inflammation and Immune Driven Condition
Servicing area
Sunshine Coast, Queensland, Buddina, Kawana, WaranaFocus areas
Pain is a major symptom of inflammation and is reported to be Australia's third most costly health condition. Pain signals activate peripheral receptors (nociceptors) which transmit pain messages along the ascending pathways of the central nervous system (CNS). Persistent or intense nociception activity con lead to distortions in neural processing, resulting in central sensitisation or pain amplification. This hypersensitivity to pain is referred to as visceral hypersensitivity which may manifest as:
- Hyperalgesia - a heightened response to painful stimulus; and
- Allodynia - a painful response to on innocuous or benign stimulus.
A more detailed look at pain transmission in the CNS shows that impulses from nociceptive stimulation trigger the release of glutamate at the dorsal horn of the spinal cord which activates neurons via N-methyl-D-aspartate (NMDA) receptors. The frequent, painful signaling stimulates the recruitment o{ more NMDA receptors into the synaptic cleft, which strengthens the spinal cords response upon repeated firing, creating o vicious cycle of nociceptive amplification.
To dampen this heightened pain signaling, the CNS is equipped with inhibitory circuits via the descending pathway;
neurons which transmit messages from the brain down the spinal cord io inhibit dorsal horn activity. Gamma-aminobutyric acid (GABA) is the chief inhibitory neurotransmitter. in the descending pathway and in addition to amplified nociceptive activity, as described above, in chronic pain disorders, there is also a concomitant reduction in GABA-mediated pain inhibition in the CNS.102 Dopamine also plays a role in promoting inhibitory pain signaling. Therefore, treatment that targets both nociception (inhibiting glutamate/NMDA) and inhibition pathways (promoting GABA and dopamine) would provide superior support than targeting either one alone.
Finally, best practice of pain management would also include ensuring key drivers of nociceptive activity are addressed, such as:
- Inflammation
- Acidity
- Ischaemia and oxidative stress
- Mitochondrial dysfunction
- Nerve dysfunction and injury
Each of these drivers stimulate the release of chemical mediates which stimulate the acid sensing ion channel (ASIC3) receptors which mediate nociception. For example, acidity (excessive free hydrogen ions [H+]), which can occur from a diet high in grains and low in fruits and vegetables, acts on ASIC to drive pain signalling. This shows that dietary manipulation may be important for pain management.
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