Symptoms And Treatment Of Peripheral Nociceptors At High Threshold Triggers Central Pathways

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1. Introduction

It is estimated that 20% of the European population suffer from chronic pain.1 The understanding of pain in research has considerably developed from the simplistic pain-gate theory.2,3 It is now understood that stimulation of peripheral nociceptors at high threshold triggers central pathways that travel via the lateral spinothalamic tract to the medulla and brainstem.4 Nociceptive information also arrives via spinoreticular and spinomesencephalic tracts; controlling autonomic, arousal and homeostatic responses.56 Sensory firing is just one influence to central pain processing. Cortical areas associated with emotional valence, memory, autonomic and motor control are all seen to activate during a pain experience supporting
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Large, fast-conducting fibres (α and β fibres) inhibit small, multi-synaptic, slow-conducting fibres (C-fibre) at the dorsal horn.13 Gaps were missing within this research due to available research resources; Noordenbos13 was unable to investigate past the spinal cord. This statement was unexplained yet it was a development in pain research. Melzack and Wall2 developed the pain-gate theory based from the research by Noordenbos13. The theory explained what Noordenbos13 was unable to prove; impulses are projected to the brain via the dorsal column, where central processes influence the activity of the gate-control system.2
Melzack3 critiqued his own research. The pain-gate was too simplistic and only explained pain as a sensory dimension.3 Rather that, pain is an output of multi-dimensional information being received and processed by a complex neural network within the brain, termed the ‘neuromatrix’.3,14,15 This guided away from the concept that pain was a sensation always produced by injury, inflammation or pathology to pain being a complex experience by multiple influences. The new explanation was also a suggestion to the nature behind some chronic pain conditions.3 Influences affecting such central processing extend from existing synaptic architecture imprinted within memory to neuro-endocrine and immunological influences.3 Despite the resources of such knowledge being

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