Abstract

Pain is a universal indicator to relinquish an association with a threatening agent, calling one into action to seek restoration and relief.  Pain manifests itself in several forms and need not correlate to identifiable stimuli.  The gate theory of pain spawned progress in new discoveries of its underlying pathophysiology and the critical effect of endorphins in the body’s natural efforts to fight pain.  Discussed are the processes of how an individual senses pain.  Additionally, types of pain examined include nociceptive, neuropathic, and idiopathic as well as chronic and acute.  Finally, the psychological state of an individual and its effect on the pain process is considered.

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Pain is a primitive component of humanity, integrating itself at all stages of life regardless of cognitive development.  Whether one is highly educated, or severely impaired, similar pain stimuli can produce identical responses, both in reflex and deterrence.   Yet despite its fundamental core, science still has much to research before coming to a full understanding of the pain process.   Throughout human history, theories on the process of pain and its management have been numerous and varied.  The ancient Greeks debated whether pain was felt in the head or the heart, and some even believed that the gods shot arrows at individuals, which resulted in painful disease (Scarborough, 1969).  Descartes, in 1644, compared the process of pain to someone standing at the bottom of a tower and pulling on a rope, striking a bell at the top (Sarason & Sarason, 2005, p 221).   While different civilizations have had their own prominent theories on the causes and treatments of pain, science nonetheless continues to strive forward to reach a unified answer to managing and understanding one of the greatest horrors that has plagued humanity, namely, the suffering of pain.  Currently, modern medicine identifies three primary types of pain: nociceptive, idiopathic, and neuropathic.  While there are clear delineations in each type, there has yet to be a full understanding of them.   Even today, for example, Scadding (2004) notes that there does not exist a uniformly accepted definition of neuropathic pain, illustrating the limitations in modern understanding of its underlying pathophysiology.

The Gate Theory of Pain

Originally proposed in 1965, Wall and Melzack described a synapse in the spinal chord that modulates or “gates” the flow of pain to the brain.  They postulated the idea of a group of second order neurons that basically “spool” incoming pain signals, upon which, once a certain minimum threshold of excitement is exceeded, the theoretical “gate” opens, sending the signals to higher order processing centers in the brain.  This theory birthed out of their observations of patients that were impervious to pain during the insertion of a needle while undergoing acupuncture.  They speculated similarly, that since the gate at the second order neuronal site of the spinal chord could allow pain to flow by “opening,” conversely certain triggers could cause the brain to turn off pain by sending impulses down the spinal chord, and closing the pain gate.  This theory led to an important discovery about pain, namely that incoming pain signals are subject modulation, increasing and decreasing, greatly changing the final perception of its degree by the patient (Choderrer & Choiniere, 2000). 

Prior to the introduction of the gate theory of pain, neuroscientists had already known the importance that chemicals had on conducting nerve signals.  The gate theory was instrumental in stimulating a rush of new research in pain pathophysiology, or pain pathways.  In addition, it gave rise to research in neurotransmitters and their abilities to excite or inhibit the ability of a cell to generate an electrical impulse.  The eventual discovery of endorphins, the brain’s natural pain suppressing compound, was a major one that gave credence to the gate theory (NIH, 1997).   Endorphins are endogenous opioid compounds and are produced by the brain, working as natural painkillers.  Cumulative research from the American Medical Association states that the work of these compounds play a crucial role in pain modulation by limiting the amount of impulses transmitted to the brain through the act of binding to special subsets of receptors, which limit the amount of pain signal that is allowed to reach the brain.  Nerve cells are equipped with opiate receptors, and when activated, the postsynaptic cell loses its ability to freely transmit signals across the synaptic gap, thus inhibiting pain.   What this means, in essence, is that the response of endorphins indeed function as a kind of ‘gate’ similar to the one originally theorized by Wall and Melzack, in that they can ‘close’ the pain pathway. 

Neurotransmitter Modulation of Pain

McCaffrey, Frock, & Garguilo (2003) describe neurotransmitters as endogenous chemical messengers that affect the perception of pain, responding to compounds such as serotonin, norepiniephrine, endorphins and substance P.   Substance P is a neurotransmitter that functions directly in the transmission of pain impulses especially involved in the modulation of inflammatory and immune responses.  Along with substance P, the aforementioned compounds all act similarly as ‘neuromodulators’ that regulate pain.  Serotonin and norepiniephrine contribute to modulation by being responsible for both inhibitory and excitatory functions within the pons and medulla areas of the brain (Pert, 1997).  In other words, depending upon their levels of release, they have the ability to both increase and decrease the level of pain felt by the individual.

As previously mentioned, endorphins are a powerful ally in a person’s natural ability to fight pain.  Chemically, endorphins are a protein, and compose a class of several times.  These proteins are able to bind to the opiate receptors on nerve cells, blocking the release of substance P and the action of those cells, which ultimately lessens the severity of pain felt by the individual.  As a result, the higher amount of endorphins released in the body, the less pain an individual will suffer.  Along with pain, pleasurable experiences such as laughing, touching, or being outside on a nice day also releases endorphins.  Drugs such as morphine and codeine are effective painkillers because they bind to the same opiate receptors as endorphin, acting in a similar fashion. 

Sensing Pain

The sensation of pain results from the firing of specialized first order neurons called nociceptors that transmit signals carried into the central nervous to nociceptive cells, forming connections to second order spinal neurons, eventually leading to the brain (McCleskey, 2003).  Once reached by the brain, third order neurons originating in the thalamus transmit the signals into the cerebral cortex, thus the sensation of pain.  Nociceptors, when functioning normally, have a much higher threshold than other sensory receptors, which can trigger at the slightest touch of a feather.  This, of course, is a good thing, as it would be hard to imagine something as gentle as a soft breeze being physically painful (types of neuropathic pain, however, can produce exactly this). When a noxious stimulus, defined as any stimulus that produces pain, is received by the peripheral pain receptors exceeding this threshold, an action potential is created that initiates the traversing of signals across the pain pathway, which ultimately results in the sensation of pain.  

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