Pain is an integral part of life. It is an everyday neural process which has the potential to teach individuals and groups. It has be understood, misunderstood and misinterpreted for years. Business, Professions and Religions have been influenced and in some cases built on the concept of pain. In this article we review the anatomical and physiological changes which occur in the body when pain is occurring to get a better understanding of the issues surrounding pain, before next month’s follow-up article looking at the overall concepts surrounding pain, pain management and the cognitive interpretation of individuals.
The imposition of stimuli upon the body from internal or external influences has the capacity it to generate the sensation of pain. The stimuli are carried through from the place of concern via the Peripheral Nervous System to the Central and Autonomic Nervous Systems; this process of tissue damage being communicated to the brain is known nociception and is assisted via nociceptors attached to mylinated axon and unmylinated C fibres. There are a number of strong stimuli which can activate nociceptors through inflammatory or biomecular stimulation within a localized environment.
The instigation of nociception may not necessarily cause the sensation of pain but in most circumstances it will. A comparison can be drawn to the circumstance of those who undergo significant trauma, such as a car accident, who may appear to be in a stoic painless state. Alternatively those individuals with functional pain syndromes may exhibit strong pain symptoms despite the presence of very little, if any tissue damage.
Perception of pain will occur when axon fibres are stimulated creating a sharp or prickling sensation, furthermore if strong enough the pain can elicit a burning pain which may last after the stimuli has stop due to the activation of C fibres. The areas of the brain associated with subjective cognition of pain experienced include regions of the cerebral and cingulated cortex which process somatosensory input and relay neural impulses which influence pain perception and nociception.
Pain processing can be divided into two phases;
The First Phase is known as “fast pain” which is immediate and less intense than that of the second phase.
The Second Phase or Slow Pain is a less localized, more unpleasant and communication delayed pain.

All nociceptors send information via a excitatory neurotransmitter known at glutamate and can be activated by either mechanical, chemical or thermal stimuli, with the addition of an “inflammatory brew” being secreted at the initial site of injury. The Inflammatory Brew comprises of a number of neurotransmitters, neurotrophins, lipids and peptides which has the potential to increase or decrease nociceptors activation thresholds; and initiate neurogenic inflammation as a result of afferent signal transmission to the dorsal horn of the spinal cord.
Neurogenic Inflammation is responsible for vasodilation, leaking proteins and fluids into the extracellular area in close proximity to the inflammatory brew and stimulating immune cells which may contribute to said inflammatory brew. This process is activated via nociceptor neurotransmitter release from peripheral terminals. As a result the local environment changes due to neurochemical presentation and both Axon and C fibres increase creating peripheral sensitisation.
Following this occurrence nociceptive signal transduction occurs along the spinothalamic tract resulting in an increased release of noreponephrine, which is projected to the thalamus and thus, nociceptive information is relayed to the hypothalamus, hippocampus and somatosensory cortex.
At the same time, pain processing may be inhibited as a result of opiod receptor stimulation by endorphins, dynorphins or enkephalin causing analgesia; this process is controlled via the Descending Central Modulation of Pain.

The Descending Central Modulation System influences nociceptive input from the spinal cord. The brain structures involved with this process coordinate activity and changed nociceptive signals via descending projections to the spinal dorsal horn, by coordinating this process the central nervous system has the ability to selectively control signal transmission from specific areas of the body.
It is believed that central modulation may have been preserved within the human evolution because of its potential adaptive effects for survival. This can be seen in traumatic events such as war where an extremely injured soldier may benefit from pain suppression in order to remove themselves from danger. However, neurobiological bonding between a number of vital structures develop a physiological pathway which can allow negative emotions or stressors to amplify or increase pain duration lending to functional deficit or suffering.

Conclusion
Pain is a very complicated, intricate and still misinterpreted phenomenon which is difficult and dare I say impossible to objectively measure. That which is measured in pain associated studies is more commonly the amount of tissue damage present or change in chemical compounds of the tissue. However, this rarely is correlated with the pain felt by an individual. The anatomical and physiological processes in an otherwise health human will be somewhat identical but, the way in which that individual interprets and therefore reacts to the stimuli may be complete over the top or under-welling leading to further injury. This is where real interest develops and can be used to explain why treatments, preventions and interventions need to be individualized to each patient rather than a stock standard protocol which can be used broadly.

In the next article we delve further into the concepts of pain, including a link to one of the most influential academics in the field of pain explanation and pain procession Dr. Lorimier Mosely.

Jackson McCosker
Director /Chief Editor

References

Garland, E. L. (2012). Pain Processing in the Human Nervous System. Primary Care Clinic and Practical .